Whiplash Injuries

Whiplash
Injuries
Diagnosis and Treatment
Second Edition
Dario C. Alpini · Guido Brugnoni

Antonio Cesarani Editors
Whiplash Injuries
Dario C. Alpini • Guido Brugnoni
Antonio Cesarani
Editors
Whiplash Injuries
Diagnosis and Treatment
Second Edition
Editors
Dario C. Alpini Antonio Cesarani
ENT-Otoneurology Service Department of Clinical Sciences and
IRCCS “Don Carlo Gnocchi” Foundation Community Health
Milan University of Milan
Italy Milan
Italy
Guido Brugnoni
Italian Academy of Manual Medicine Audiology Unit
Italian Institute for Auxology IRCCS “Ca’ Granda” Ospedale Maggiore
Milan Policlinico
Italy Milan
Italy
ISBN 978-88-470-5485-1 ISBN 978-88-470-5486-8 (eBook)

DOI 10.1007/978-88-470-5486-8
Springer Milan Heidelberg New York Dordrecht London
Library of Congress Control Number: 2014932997
© Springer-Verlag Italia 2014

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Foreword
I have dedicated my early researches to the study of learning disturbances and

behavioral disorders in childhood, especially with regard to autism. The focus of my
study was on the correlation between posture, that is the language of the body, and
mental health. During my fellowship at Stanford University in the 1970s, I devel-
oped the idea that measurement of postural control might be the best way to inves-
tigate cognitive functions. The basic posture of the human being is upright
bipedalism; maintaining dynamic equilibrium of the body, which is like an inverted
pendulum on a relatively restricted base area, is an evolutionary phenomenon
directly linked to high-level cognitive development. In adulthood, maintaining
stance is perceived to be easy, at least under normal conditions on steady surfaces,
but it actually requires a very high level of sensorimotor control to allow a low-
effort antigravitary alignment of the different parts of the body.
One of the major positive aspects of an upright position is the possibility of hav-
ing an improved perception of the environment. In the horizontal plane, the atlanto-
occipital joint enables a wide range of head movement, thus allowing the eyes to
explore further. The relatively limited support base allows the body to turn rapidly
in order to control the environment behind us. In the vertical plane, the lumbosacral
spine allows the extension of the head and the trunk in order to explore the environ-
ment over our head. Thus, the human posture is an evolution from the quadrupedal
motion, offering tremendous possibilities exploring the environment along the three
space axes.
The posturographic equipment I developed in the 1970s I called tetra-ataxiometry
because it records simultaneously the pressures exerted on the ground by the four sup-
ports: right and left toes and right and left heels. It also allows investigating how the free
movement of the neck during rotation, extension, and flexion influences the control of
the upright position. In other words, the equipment lets us to investigate how abilities
that were specific to human beings correlated with motor programs specific to quadru-
peds. In the phylogenesis, bipedal posture was relatively recently implemented on qua-
drupedal motor control, and this can be retraced by observing how a child fights against
the force of gravity in the early years of life.
This concept explains the pathogenesis of whiplash associated disorders (WADs)
that frequently cause impairments not proportionate to the intensity of the impact.
The relatively low energy transferred to the body during an accident specifically
affects the two most phylogenetically recent parts of the body – the atlanto-occipital
v
vi Foreword
joint and the lumbosacral spine – thus limiting the ability of the body to rotate the
head and to extend the head and the trunk. In other words, the whiplash effect makes
the human body akin to that of primates. This probably reveals the biological and
social importance of WADs.
This second edition is primarily based on the evolutionary concepts of the ves-
tibular system, originating in quadrupeds and advanced in bipeds. The vestibular
system supports, in an entirely unique way, perceptual orientation, dynamic body
stabilization, retinal image stabilization, and autonomic nervous functions.
This book discusses the different aspects of whiplash, a particular kind of trauma
that has a significant impact on the body as a whole. In WADs, pain is an important
aspect, but it is only one of the effects, with functional ones being more prevalent.
This book is therefore particularly interesting and complete as it focuses both on the
painful and the functional aspects of WADs.
Prof. Reuven Kohen-Ratz,

Professor Emeritus of Special Education – Hebrew
University of Jerusalem
Jerusalem, Israel
Preface to Second Edition
The incidence of whiplash injuries has been estimated to be 1/1,000 people per year
in the Western world. Chronic spine pain and associated symptoms following whip-
lash injury cause severe individual burdens of disease and high costs of healthcare
systems at least in the Western countries (with the exception of Lithuania and
Greece due to specific approach of health system and insurance companies to whip-
lash associated disorders in these countries).
The first edition of this book was prepared one year before that the Quebec Task
Force (QTF) presented the first classification of whiplash associated disorders
(WADs). QTF guidelines are still widely accepted both for diagnosis and
treatment.
Furthermore, evidence based medicine (EBM) became more and more important
in these last 10 years in leading clinicians toward the most effective approach to
diseases and disorders, including WADs. However, whiplash mechanism is so com-
plicated to lead to complex disturbances that very frequently they are very difficult
to simplify into EBM tracks.
The term “whiplash” dates back to 1928, when the American physician
H.E. Crowe used it in a symposium of traffic accidents held in San Francisco. Crowe
did not refer to the injury as such, but as the motion of the head and neck that under-
went in conjunction with a collision.
The interaction between the accident and the human body is not simply a
mechanic interaction. In contrast to mechanical systems in which component parts
interact linearly to produce a predictable output, the components of complex sys-
tems interact nonlinearly over multiple scales and produce unexpected results. The
output of mechanical systems can be controlled by manipulating each one of its
parts, while the output of complex systems is dynamic, behaving differently accord-
ing to initial conditions and feedback. This is the case of whiplash and WADs.
In order to minimize the risk of long-term problems among people with acute
whiplash injury, concurrently acute stress disorder (ASD) and/or posttraumatic
stress disorder (PTSD) should be diagnosed and adequately treated.
For the above complex reasons, we thought to be necessary an updating of the
first edition that takes into account the different challenges to whiplash, the most
updated EBM diagnostic and therapeutic indications, and the evolution of QTF
guidelines.
vii
viii Preface to Second Edition
More specifically, in this edition, the Editors tried to include all the pathological
effects of whiplash and not just the traditional neck and spine effects. The leading
idea of this book is the conception of whiplash as a trauma of the body as a whole,
obviously with different impact on the different parts of the body. The second lead-
ing idea is that the effects of whiplash are substantially unpredictable per se and thus
a brain damage has to be expected just like a temporo-mandibular joint disorder or
low back pain.
Some problems have been encountered in updating the chapter dedicated to med-
ico-legal aspects. Various studies on how possible insurance compensation may
influence the course of whiplash injuries have produced diverging results. Generally,
however, there is no evidence indicating any significant difference in the results
between those who have applied for such compensation and those who have not.
Furthermore, a common legal procedure about compensation of whiplash inju-
ries in the different countries of the Western world is lacking. For these reasons we
focused on management and treatment of patients disorders, but we avoided to
include a chapter about medico-legal aspects of WADs.
Finally, we can state that the spirit of this second edition is paying our attention
to collect in this book What’s new – What else besides pain – What to do for patients
affected with WADs.
Dario C. Alpini
Milan Guido Brugnoni
Milan, Italy Antonio Cesarani
November 2013
Preface to First Edition
This book is based on the proceedings and discussions of a closed workshop held in
Santa Margherita Ligure in January 1995.
It was an original scientific experience: no public was admitted. For 3 days the
main contributors of this book remained closed in a wonderful hotel.
At the same hotel in the 1930s, Guglielmo Marconi performed his first experi-
ments with radio waves. The hotel was therefore an ideal place, although the prob-
lems we discussed were not so “revolutionary” like Marconi’s experiments.
On these days round tables, we performed highly restricted meetings on specific
topics and presentation of selected papers, only for very few persons, were
performed.
Discussions were on definition, ethiopathogenesis, physiopathology, clinical and
instrumental evaluations, and medicolegal and therapeutic aspects of whiplash
injuries.
All the attendants tried to report and discuss personal experiences and ideas in
order to compare them.
All the discussions were especially aimed to prepare the chapters you will read
in this book.
We returned to our homes very tired, but very rich in our minds. We really hope
that after reading this book you will be as tired as rich.
We are very grateful to Pharmacia, who supported the closed workshop and the
preparation of this publication.
Antonio Cesarani
Milan, Italy Dario C. Alpini
ix
Contents
1 Whiplash: An Interdisciplinary Challenge . . . . . . . . . . . . . . . . . . . . . 1

A. Cesarani, C.F. Claussen, and D.C. Alpini
Part I General Aspects
2 Epidemiology of Whiplash-Associated Disorders . . . . . . . . . . . . . . . . 13

F. Ioppolo and R.S. Rizzo
3 Functional Anatomy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
C.L. Romanò, A. Mondini, S. Brambilla, and F. Ioppolo
4 Kinematics and Dynamics of the Vehicle/Seat/Occupant
System Regarding Whiplash Injuries . . . . . . . . . . . . . . . . . . . . . . . . . 27
P.L. Ardoino and F. Ioppolo
5 Whiplash Lesions: Orthopedic Considerations. . . . . . . . . . . . . . . . . . 43
E. Meani, S. Brambilla, A. Mondini, C.L. Romanò,
and F. Ioppolo
6 Neurology of Whiplash . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
G. Meola, E. Bugiardini, and E. Scelzo
7 Radiological Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
A. Bettinelli, M. Leonardi, E.P. Mangiagalli, and P. Cecconi
Part II Pathophysiology
8 The Vestibulo-vertebral Functional Unit . . . . . . . . . . . . . . . . . . . . . . . 77

D.C. Alpini, G. Brugnoni, A. Cesarani,
and P.M. Bavera
9 Pathophysiology of Whiplash-Associated Disorders:
Theories and Controversies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
M. Magnusson, M. Karlberg, C. Mariconda, A. Bucalossi,
and G. Dalmazzo
xi
xii Contents
10 The Contribution of Posturology in Whiplash Injuries . . . . . . . . . . . 95

P.M. Gagey, D.C. Alpini, and E. Brunetta
11 Whiplash-Associated Autonomic Effects . . . . . . . . . . . . . . . . . . . . . . . 107
R. Boniver, D.C. Alpini, and G. Brugnoni
12 Whiplash-Associated Temporomandibular
Disorders (TMDs) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
E. Brunetta
13 Whiplash and Sport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
M. Albano, D.C. Alpini, and G.V. Carbone
14 Whiplash Associated Somatic Tinnitus (WAST) . . . . . . . . . . . . . . . . . 139
D.C. Alpini, A. Cesarani, and A. Hahn
Part III Evaluation
15 Anamnesis and Clinical Evaluation of Whiplash-Associated

Equilibrium Disturbances (WAED) . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
A. Cesarani, D.C. Alpini, D. Brambilla,
and F. Di Berardino
16 Whiplash Effects on Postural Control . . . . . . . . . . . . . . . . . . . . . . . . . 165
M. Magnusson and A. Hahn
17 Static Posturography and Whiplash. . . . . . . . . . . . . . . . . . . . . . . . . . . 171
P.L. Ghilardi, A. Casani, B. Fattori, R. Kohen-Raz,
and D.C. Alpini
18 Dynamic Posturography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
S. Barozzi, B. Monti, D.C. Alpini, and F. Di Berardino
19 The Cervico-Cephalic Interaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
D.C. Alpini, V. Mattei, D. Riva,
and F. Di Berardino
20 Neurotology in Whiplash Injuries: Vestibulo-ocular
Reflexes and Visuo-vestibular Interaction . . . . . . . . . . . . . . . . . . . . . . 213
L.M. Odkvist, A. Cesarani, and F. Di Berardino
21 Vestibular Evoked Potentials in Relapsing Paroxysmal
Positional Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
F. Di Berardino, D.C. Alpini, L. Pugnetti,
V. Mattei, and B. Franz
22 Whiplash Effects on Brain: Voluntary Eye Movements. . . . . . . . . . . 233
M. Spanio, S. Rigo, and D.C. Alpini
Contents xiii
23 Whiplash Effects on Brain: Optokinetic Nystagmus

and Visuo-Vestibular Interaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
A. Salami, M.C. Medicina, and M. Dellepiane
24 Abducting Interocular Ophthalmoplegia
After Whiplash Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251
D.C. Alpini, A. Cesarani, and E. Merlo
Part IV Treatment
25 Pharmacological Treatment of Whiplash-Associated

Disorders (WAD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259
E.A. Pallestrini, E. Castello, G. Garaventa, F. Ioppolo,
and F. Di Berardino
26 Physiotherapy of Neck, Back and Pelvis . . . . . . . . . . . . . . . . . . . . . . . 269
I. Odkvist, L.M. Odkvist, S. Negrini, and C. Mariconda
27 Manual Medicine in Whiplash-Associated
Disorders (WAD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
G. Brugnoni, C. Correggia, and C. Mariconda
28 Rehabilitation Strategy According
to the Quebec Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291
S. Negrini, P. Sibilla, S. Atanasio, and G. Brugnoni
29 Whiplash-Associated Equilibrium Disturbances
(WAED) Rehabilitation: Vestibular Re-education
and Vestibular Rehabilitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
D.C. Alpini, A. Cesarani, and F. Di Berardino
30 Vestibular Electrical Stimulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315
A. Cesarani, D.C. Alpini, and E. Filipponi
31 The Neurophysiological Basis of Vestibular
Electrical Stimulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321
M. Osio, L. Brunati, G. Abello, and A. Mangoni
32 Ski Trainer Oscillating Platform:
Proprioceptive Reeducation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327
M. Savini, D.C. Alpini, and A. Cesarani
33 Visual Feedback Postural Control Re-education . . . . . . . . . . . . . . . . 333
D.C. Alpini, A. Cesarani, M. De Bellis,
R. Kohen-Raz, and D. Riva
34 Neurorehabilitation of Ataxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
M. Forni
xiv Contents
35 Rehabilitation in Polytrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351

E. Spadini
36 Acupuncture and Chinese Medicine: Cervical Disorders
and Chronic Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355
G. Garozzo
37 Acupuncture and Chinese Medicine:
Equilibrium Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 373
P.L. Ghilardi, C. Borsari, A. Casani, L. Bonuccelli,
and B. Fattori
Part V Conclusive Remarks
38 Management and Treatment of WAD Patients:

Conclusive Remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
D.C. Alpini, G. Brugnoni, and A. Cesarani
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401
Whiplash: An Interdisciplinary
Challenge 1
A. Cesarani, C.F. Claussen, and D.C. Alpini
Definitions of whiplash syndrome are controversial. Generally speaking, the

syndrome comprehends symptoms following a traffic accident, usually a rear-end
collision. These symptoms are varied and variably combined:
• Orthopedic, such as neck pain and functional limitation of cervical movements
• Neurological, such as paresthesias
• Audiological, such as tinnitus and hypoacousia
• Otorhinolaryngological, such as dysphagia and dysphonias
• Equilibriometric, such as vertigo and dizziness
• Odontoiatric, such as disturbances of occlusions and temporomandibular joint
pain
• Neuropsychological, such as anxiety and attentional disturbances
The term whiplash was used for the first time in 1928 and included several mech-
anisms. For example, the kinematics of the head-neck movements are different in
rear-end collisions than in side collisions, and it is different for the driver rather than
the passenger. It is also different if the subjects wore safety belts or not.
Thus, the first challenge is definition. In this book, whiplash injury can be defined
as a noncontact quick (« 50 ms) acceleration-deceleration head-neck trauma [1–3].
A. Cesarani
Department of Clinical Sciences and Community Health,
University of Milan, Milan, Italy
Audiology Unit, IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico, Milan, Italy
e-mail: antonio.cesarani@unimi.it
C.F. Claussen
Neurootologic and Equilibrium Society (NES), Bad Kissingen, Germany
e-mail: claussensology@gmx.de
D.C. Alpini (*)
ENT-Otoneurology Service, IRCCS “Don Carlo Gnocchi” Foundation, Milan, Italy
e-mail: dalpini@dongnocchi.it
D.C. Alpini et al. (eds.), Whiplash Injuries, 1

DOI 10.1007/978-88-470-5486-8_1, © Springer-Verlag Italia 2014
2 A. Cesarani et al.
Table 1.1 Abbreviated AIS-Code Injury

injury score (AIS)
0 No injury
1 Minor
2 Moderate
3 Serious
4 Severe
5 Critical
6 Maximum
9 Not further specified (NFS)
The different combinations of symptoms lead to different syndromes so described

in the literature: cervical syndrome, traumatic cervical syndrome, cervico-cephalic
syndrome, and cervicobrachial syndrome.
Generally, all syndromes are characterized by a plethora of functional symptoms
and lack of sufficient objective morphological findings. Either for diagnosis or for
therapy, different specialists and examinations are usually necessary; however, visit
to different specialists usually leads to different “specialized” diagnosis and
treatments.
The second challenge is gathering documentation of the functional and morpho-
logical basis for the patient’s complaints. Documentation is indispensable for medi-
colegal expertise and/or for treatment planning.
Due to the complexity and the wide differences of the legal system regarding
insurances’ approach to WAD, this reedition explains how to document WAD in
patients but not how to use this documentation for medicolegal expertise. In this
way, medicolegals of the different countries can adapt our information in their spe-
cific field of application.
Since a patient’s complaint is caused by the trauma that lasts for months and can
persist for years, the third challenge is an interdisciplinary approach to the treatment
in order to avoid chronic impairment and over specialized therapy.
Whiplash injuries vary from minor to severe. They can be classified according to
the Abbreviated Injury Score (Table 1.1). Generally, the evolution of whiplash is
divided into three phases:
1. The onset phase, involving local reactions with release of neuromediators such
as serotonin, histamine, bradykinin, and classical inflammation [4]
2. The recovery phase, locally characterized by synthesis of new collagen fibers
3. The remodelling phase, in which the neck and the body modify their positions
and movement strategies in order to restore normal daily life activities
During whiplash, the kinematics of the cervical spine is completely disrupted
(Fig. 1.1). During the impact, the vertebrae do not reciprocally move harmonically
such as during physiological antero- and retroflexion of the neck. Whiplash is char-
acterized by transient, but not always temporary, reciprocal inversions of the differ-
ent cervical segments [5–7]. For example, in the last phase of anteroflexion,
inversions in segments CI–C2 and CO–Cl have been observed, while in the second
phase of retroflexion, an inversion of the segment CO–Cl happens [8, 9]. The recip-
rocal inversions lead to ligament and soft tissue lesions, with a segmental
1 Whiplash: An Interdisciplinary Challenge 3
Antiflexion
a
Retroflexion
=a =b =c =d
Fig. 1.1 Modification of reciprocal positions of cervical spine segments during antero-(a) and
retroflexion (b) in whiplash mechanisms. In the initial phase of anteroflexion Cl–C2 and CO–C2
invert their position (a). In the second phase of retroflexion, inversion of CO–Cl is observed. a:
flexion; b: extension; c: sequence; d: inversion symptoms
dysregulation causing a specific activation of nociceptive inputs and consequent

somatomotor and sympathetic-motor dysfunctions [1]. The nociceptive inputs, via
interneurons and alpha-motoneurons, provoke a dysregulation of motoneurons for
the flexors and extensors leading to an asymmetrical hypertonus. The latter [10, 11]
is generally observed in the trapezius and sternocleidomastoid with consequent
compression of the accessorius nerve, and in scaleni with compression of the bra-
chial plexus, responsible for paresthesias. The dysregulation of the orthosympa-
thetic cervical system causes activation of vasoconstrictive subsystems, not always
localized to the involved segments. Vasoconstriction induces dystrophic impairment
contributing to the cervicofacial and cervicobrachial symptoms.
The ganglion cervicalis superius is localized at the CI–C4 segment and inner-
vates the neck and upper respiratory and digestive tracts [12].
The cervicobrachial sympathetic complex from C5 to Th1, along with the post-
ganglionate synapses in the cervical medius ganglion (C5–C6) and inferius (C7–
C8), innervates the medium parts of the respiratory and digestive tracts.
Cervico- and craniospinal injuries during acceleration-deceleration lead to head/
neck proprioception disruption causing transient, sometimes permanent, abnormal
proprioceptive information regarding the reciprocal position of the neck, head, and
trunk. In Fig. 1.2, the so-called spinocerebello-vestibulospinal circuitry is shown.
General proprioception information (from muscles, ligaments, and joints) is inte-
grated and elaborated in the cerebellum together with special proprioception infor-
mation from maculae and cristae. From the cerebellum, efferent pathways return to
spinal motoneurons through another elaboration in the vestibular nuclei (with spe-
cial regard to the lateral Deiter’s nucleus) [13–16].
1 2
3
1 Area 2v
2 Area 3a
3 Nucleus ventralis posterolateralis
4 4 Nucleus ventralis posterior inferior
5 5 Nucleus interstitialis rostralis of the
6 FLM
6 Nucleus interstitialis of Cajal
7 8 9 7 Tractus interstitiospinalis
10 Special 8 Nucleus nervi oculomotorii
11
12
proprioception 9 Tractus vestibulothalamicus
13 from cristae 10 Nucleus nervi trochlearis
14 and maculae 11 Tractus vestibulomesencephalicus
15 12 Fasciculus longitudinalis medialis
16
(FLM)
13 Cerebellum
14 Pendunculus cerebellaris inferior
19
18 15 Nucleus nervi abducentis
16 Nucleus vestibularis superior
20 17 Nucleus vestibularis lateralis
21 18 Nucleus vestibularis medialis
22 19 Nucleus vestibularis inferior
23 20 Nucleus prepositus hypoglossi
12 21 Nucleus ilivaris inferior
7 22 Tractus vestibulospinalis medialis
23 Tractus vestibulospinal lateralis
General
proprioceptive
inputs
Fig. 1.2 The connections of the vestibular system: efferent connections of the vestibular nuclei
and the spinocerebello-vestibulospinal circuitry
This circuitry is the anatomo-neurophysiological basis needed to understand

why an apparent segmental injury often becomes an injury of the whole individual.
Equilibrium disorders can be directly caused by perturbation of the integration of
general and special proprioception due to abnormal peripheral inputs from the neck
or for central dysfunction, particularly of the brainstem [17–20].
Whiplash is a true head trauma even if there is no contact of the head with an
object. Cerebral contusions or intracranial bleeding are extremely rare, but abdu-
cens mono and bilateral palsy [21] and laryngeal palsy have been described [22].
Neurovegetative symptoms and affective-cognitive symptoms are as frequent as in
post-commotional syndromes and are characterized by hyperesthetic emotional and
neuroasthenic symptoms including tinnitus, dysphasia, nausea, unsteadiness, and

vertigo [23–29].
True neuropsychological disorders are frequent after whiplash. Typically, espe-
cially 6–8 months after the trauma, psychological symptoms appear: restlessness,
nervousness, anxiety, emotional instability, difficulties in concentration, and depres-
sion. In 15–25 %, this neuropsychological syndrome can evolve chronically and can
be misdiagnosed as an “indemnity syndrome.” Experimental postmortem studies
showed focal contusions in frontal and temporal cortex, corpus callosum, subcorti-
cal structures, diencephalon, and subdural and subarachnoid microbleeding as con-
sequences of sudden angular accelerations. Rarely, alterations are macroscopic,
while generally, microscopic lesions have been revealed [30–33].
One of the central networks involved in post-whiplash disorders is the ascending
reticular activating system (ARAS). Experimental studies showed involvement of
the ARAS especially for transitory accelerations. In Ommaya’s hypothesis [34, 35],
the centripetal forces during acceleration-deceleration lead to an abnormal stretch-
ing of the cerebrum with, furthermore, a sudden transient increase of the pressure of
the cerebrospinal fluid [36]. In this hypothesis, whiplash provokes a commotio cere-
bri with potential injuries of temporal cortex, amygdala, hippocampus, medial tem-
poral cortex, corpora mamillaria, medial thalamus, basal nuclei, prefrontal cortex,
and retrosplenial cingulate cortex. All these structures may be involved in the gen-
esis of neuropsychological symptoms [2, 37, 38].
The cerebral effects of whiplash have been studied also by electroencephalogra-
phy (EEG). After a period ranging from 1 to 9 years in patients with a chronic
whiplash syndrome, EEG alterations have been observed with percentages ranging
from 30 to 49 %.
Glucose cerebral metabolism has been investigated by positron-emission tomog-
raphy (PET) [39], and alterations have been shown in the frontal and temporal cor-
tex and in nucleus caudatus. Lesions of frontal cortex are responsible for attentional
disorders.
Pathogenesis of otoneurological disorders is still debated and includes the fol-
lowing explanations:
• Mechanical compression with dynamic stenosis of the vertebral artery
• Sympathetic abnormal stimulation
• Proprioceptive disorders especially from the cervical and lumbar regions
[40, 41]
• Central vestibular system disorder
Probably, equilibrium disorders derive from different combinations of different
mechanisms. The kinematics of the acceleration-deceleration are different, for
example, for the driver, who usually opposes the trauma by means of his/her arms
on the wheel, and the passenger, who usually receives, completely and passively,
the impact forces. Differences can be observed if patients did or did not wear safety
belts during the impact: with safety belts the movement of the head and the neck is
not sagittal but torsional with the first dorsal vertebra as fulcrum. The sense of the
torsional component is different: clockwise for the passenger, counterclockwise for
the driver. Furthermore, the impact is rarely caused by a perfect sagittal rear-end
collision, while very often, the impact causes a rotational acceleration of the car.
Torsional and angular accelerations cause microlesions in different parts of the
brain, and this can lead to different combinations of signs and symptoms in the so-
called whiplash syndrome [42].
Torsional and rotational acceleration-deceleration can lead to cranio-mandibular
dysfunctions, too. Computer simulations [43] showed an initial derangement of
condylus position with a myogenic secondary reaction during hyperextension and
consequent modification of the condylus position. During hyperflexion, the retropo-
sitioning of the condylus leads to a compression of the posterior ligament rich in
vessels and proprioceptors [44–47].
Following whiplash either for mechanical lesions of cervical dynamic or for
central dysfunctions, some modifications of patient posture are usually observed
[48]: the head modifies its position according to an antalgic flexion; the head
reduces its rotational and lateroflexion movements. During subject movements, the
rotation of the body is along the trunk and not the neck, the trunk is ipsilaterally
rotated with respect to the side of the lesion, the pelvis is rotated according to head
antalgic position, and the position of center of gravity (CoG) is modified. In the
months following the trauma, erector paravertebral muscles become hypotonic,
and the prevalence of flexors induces a forward displacement of the CoG facilitat-
ing forward falling. Rotation of the trunk increases unsteadiness, and forward CoG
displacement provokes a relative flexion of the legs to oppose falling and derange-
ment of normal ankle and hip strategies. In fact, Equitest shows a prevalence of
ankle strategies and delayed motor control test latencies either in backward or in
forward translations.
From a cybemetic point of view, equilibrium disorders are provoked by distor-
tion and desynchronization of the proprioceptive chain:
• Modification of the proprioceptive cervical inputs to the vestibular nuclei and
reticular formation
• Desynchronization between special vestibular inputs and general cervical inputs
regarding head position and movement
• Modification of the cervico-spinal reflexes
If desynchronizations of proprioceptive signals “force” the limits of the patient’s
equilibrium system calibration (see Chap. 29), the system is not able to adapt and it
becomes dysfunctional: vertigo and dizziness appear.
Thus, the fourth challenge is correct treatment of an apparently localized injury
that causes a systemic dysfunction. The treatment must be planned on the basis of
an accurate functional local and systemic diagnosis. In the acute phase, treatment is
aimed at reducing the impairment that is principally caused by local dysfunction. In
the immediate post-acute phase, impairment is due to the dysregulation of somatic
and vegetative reflexes at the involved spinal segment level. This dysregulation, if
not correctly treated, can lead to the so-called chronic phase of segmental impair-
ment. Further evolution of the syndrome includes non-segmental dysregulation:
primary damage induces secondary damage. The chronic syndrome can lead to dis-
ability with motor dysfunction of the patient, usually combined with vertigo and
dizziness. Rarely, motor dysfunction leads to social handicap with working and/or
attending to normal daily life activity.
Rehabilitation is generally the treatment of choice either in acute or in chronic

syndromes, and it is usually combined with drugs [49] and with both physical [50–
54] and instrumental therapies. Rehabilitation is aimed either at the treatment of the
spine or at ataxia and motor uncoordination. In the chronic phase, rehabilitation
must also include instruction for ergonomic daily life activities [55, 56].
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2. Jenkins A et al (1986) Brain lesions detected by magnetic resonance imaging in mild and
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22:1655–1660
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23. Dikmen S et al (1986) Neuropsychological and psychological consequences of minor head
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Part I
General Aspects
Epidemiology of Whiplash-Associated
Disorders 2
F. Ioppolo and R.S. Rizzo
Until recently, there was no consensus on the definition of whiplash. According to

the Quebec Task Force (QTF) on whiplash-associated disorders (WAD), “whiplash
is an acceleration-deceleration mechanism of energy transfer to the neck. It may
result from rear-end or side-impact motor vehicle collisions, but can also occur dur-
ing diving or other mishaps. The impact may result in bony or soft-tissue injuries
(whiplash-injury), which in turn may lead to a variety of clinical manifestations
called Whiplash-Associated Disorders.”[1] Patients with whiplash can be classified
by the severity of signs and symptoms: Grade 0 means no complaints or physical
signs; Grade 1 indicates neck complaints (such as pain, tenderness, and stiffness)
but no physical signs; Grade 2 indicates neck complaints and musculoskeletal signs
(such as a decreased range of motion or muscle weakness); and Grade 3 and Grade
4 indicate neck complaints and, respectively, neurological signs (such as sensory
deficit) or fracture or dislocation.
The incidence of whiplash injury varies between different parts of the world,
with rates as high as 70 per 100,000 inhabitants in Quebec [1], 106 per 100,000 in
Australia [2], and 188–325 per 100,000 inhabitants in the Netherlands [3].
Versteegen also reported a sharp increase in whiplash injuries from 1989 to 1995 in
the Netherlands, in conjunction with a more or less stable pattern of seat belt use [4].
F. Ioppolo (*)
Department of Physical Medicine and Rehabilitation,
“Sapienza” University,
Piazzale Aldo Moro 5, 00185 Rome, Italy
e-mail: francescoioppolo@yahoo.it
R.S. Rizzo
“Sapienza” University,
Piazzale Aldo Moro 5, 00185 Rome, Italy
Physical Medicine and Rehabilitation Unit,
Nomentana Hospital, Largo Berloco 1, Fonte Nuova,
Rome 00010, Italy

14 F. Ioppolo and R.S. Rizzo
Moreover, Versteegen et al. identified patients who complained of neck pain after
having been involved in a traffic accident and gone to an emergency room. Over a
20-year period, they found a tenfold increase in such visits, from an average annual
incidence of 3.4 visits per 100,000 inhabitants (1970–1974) to 40.2 visits per
100,000 (1990–1994) [5].
Richter reported an increase of whiplash injuries in drivers injured in motor vehi-
cle collisions in Hanover, Germany; these went from less than 10 % in 1985 to more
than 30 % in 1997 [6].
The cumulative incidence of patients seeking healthcare for whiplash arising
from a road traffic accident has increased during the last 30 years to recent estimates
of >3/1,000 inhabitants in North America and Western Europe [7] and between 1.0
and 3.2/1,000 inhabitants in Sweden [8].
A 1983–1984 hospital-based study from the UK (which included persons going
to the hospital for evaluation of WAD symptoms) reported an annual incidence of
WAD of 27.8 (95%CI 23.6–32.6) per 100,000 inhabitants [9]. In the UK, insurance
statistics indicate that 300,000 patients present per annum with whiplash-associated
disorders [10].
With annual North American incidence rates estimated to be between 70 and 329
per 100,000 people [1, 11], whiplash injuries are the most common injury following a
motor vehicle collision [4, 12]. Indeed, in 2000, whiplash was the most common emer-
gency room-treated motor vehicle injury in the USA [4]. In the Canadian province of
Saskatchewan, 83 % of traffic injury claims were for whiplash during 1994–1995,
giving an annual incidence of 677 insurance claims per 100,000 adult population [13].
Incidence data for WAD are based mainly on study settings such as emergency
room visits and insurance injury claims.
In literature, there are no published studies regarding the Italian epidemiology of
WAD. Thus, data collection comes from the “Casellario Centrale Infortuni,” which
includes data on damage to the person with particular reference to those covered by
“RC Auto” insurance [14].
Specifically, in 2009, there were 491,736 reports made to the CCI, 355,334 of
which involved the cervical rachis. Of these latter, 218,754 qualify for definition as
whiplash. Whiplash represented 44.5 % of all accidents.
In 2010, there was a notable decrease in the overall number of accidents and
cases of whiplash. There were 130,433 cases of whiplash, which represents 42.8 %
of all accidents.
2.1 Factors Associated with WAD
One potentially important factor for risk of WAD is the severity of impact, but no
method exists to assess this in a standardized way. However, various preventive
devices have a protective effect in passenger cars in rear-end collisions [7].
Although it seems that females are at slightly greater risk of WAD, the evidence
of gender as a risk factor for seeking healthcare or making a claim for WAD is not
consistent [15, 16].
2 Epidemiology of Whiplash-Associated Disorders 15
Younger persons (aged 18–23) seem to be at greater risk of making insurance

claims and/or being treated for WAD [13].
There is some evidence that neck pain before a collision might be a risk factor
for acute neck pain after a rear-end collision [17]. Today, there are no scientifically
admissible studies examining the effect of psychological, social, genetic, and cul-
tural factors in the onset of WAD after traffic collision [7].
2.2 Prognosis
The Quebec Task Force states that whiplash injuries have favorable prognosis and
their conclusion is that the 87 % and the 97 % of the patients recovered (recovery is
defined by authors as cessation of time-loss compensation) from their injury at 6 and
12 months after the vehicle collision, respectively. Statement and conclusion are
questionable. Whether these patients still had pain or discomfort and needed medical
care, it was not reported. A review contradicted the QTF’s conclusions that most
whiplash injuries were short-lived [18]. These authors concluded that between 14
and 42 % of the whiplash patients developed chronic complaints (longer than 6
months) and that 10 % of those had constant severe pain. Internationally, the propor-
tion of chronic complaints varies between 2 and 58 % [19, 20], but lies mainly
between 20 and 40 %. Other studies observed that the proportion of patients who
report pain and disability 6 months after the accident varies between 19 and 60 %
[21, 22].
Various studies of how possible insurance compensation may influence the
course of WAD have produced diverging results, but according to Jansen et al. [23],
there is no evidence indicating any significant differences between those patients
who have applied for such compensation and those who have not.
Regarding the economic cost due both to management of whiplash disorders and
time off work, epidemiological results are limited, but it could be estimated as $3.9
billion in the USA and €10 billion in Europe in a year [24].
References
1. Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S et al (1995) Scientific
monograph of the Quebec Task Force on Whiplash Associated Disorders: redefining ‘whip-
lash’ and its management. Spine 20(8 Suppl):8S–58S
2. Miles KA, Maimaris C, Finlay D, Barnes MR (1988) The incidence and prognostic signifi-
cance of radiological abnormalities in soft tissue injuries to the cervical spine. Skeletal Radiol
17:493–496
3. Wismans KSHM, Huijkens CG (1994) Incidentie en prevalentie van het ‘whiplash’-trauma.
TNO report 94. R.B.V.041. TNO Road-Vehicle Research Institute, Delft
4. Versteegen GJ, Kingma J, Meijler WJ et al (2000) Neck sprain after motor vehicle accidents in
drivers and passengers. Eur Spine J 9:547–552
5. Versteegen GJ, Kingma J, Meijler WJ et al (1998) Neck sprain in patients injured in car acci-
dents: a retrospective study covering the period 1970–1994. Eur Spine J 7:195–200
16 F. Ioppolo and R.S. Rizzo
6. Richter M, Otte E, Pohlemann T et al (2000) Whiplash-type neck distortion in restrained car

drivers; frequency, causes and long-term results. Eur Spine J 9:109–117
7. Holm LW, Carroll LJ, Cassidy JD et al (2008) The burden and determinants of neck pain in
Whiplash associated disorders after traffic collisions, results of the Bone and Joint Decade
2000–2010 Task Force on Neck pain and its Associated Disorders. Spine 33(4 Suppl):S52–S59
8. Jansen GB, Edlund C, Grane P et al (2008) The Swedish Society of Medicine and the Whiplash
Commission Medical Task Force. Whiplash injuries: diagnosis and early management. Eur
Spine J 17(Suppl 3):S359–S418
9. Otremski I, Marsh JL, Wilde BR et al (1989) Soft tissue cervical spinal injuries in motor
vehicle accidents. Injury 20:349–351
10. Burton K (2003) Treatment guidelines: is there a need? In: Proceedings of Whiplash
Conference 2003, Bath, England, 6–8 May. Lyons Davidson Solicitors, Bristol
11. Quinlan KP, Annest JL, Myers B, Ryan G, Hill H (2004) Neck strains and sprains among
motor vehicle occupants – United States, 2000. Accid Anal Prev 36:21–27
12. Berglund A, Alfredsson L, Jensen I, Bodin L, Nygren A (2003) Occupant-and crash-Related
factors associated with risk of whiplash injury. Ann Epidemiol 13:66–72
13. Cassidy JD, Carroll LJ, Côté P et al (2000) Effect of eliminating compensation for pain and
suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 342:
1179–1186
14. Il Casellario Centrale Infortuni, Rapporto Statistico (2011) http://casellario.inail.it/repository/
ContentManagement/information/N115396216/RapportoStatisticoCasellario2011.pdf
15. Bjornstig U, Hildingsson C, Toolanen G (1990) Soft-tissue injury of the neck in a hospital
based material. Scand J Soc Med 18:263–267
16. Bring G, Bjornstig U, Westman G (1996) Gender patterns in minor head and neck injuries: an
analysis of casualty register data. Accid Anal Prev 28:359–369
17. Obelieniene D, Schrader H, Bovim G, Miseviciene I, Sand T (1999) Pain after whiplash: a
prospective controlled inception cohort study. J Neurol Neurosurg Psychiatry 66(3):279–283
18. Barnsley L, Lord S, Bogduk N (1994) Whiplash injury: clinical review. Pain 58(3):283–307
19. Coté P, Cassidy JD, Carroll L, Frank JW, Bombardier C (2001) A systematic review of the
prognosis of acute whiplash and a new conceptual framework to synthesize the literature.
Spine 26:E445–E458
20. Scholten-Peeters GGM, Verhagen AP, Bekkering GE, van der Windt DAWM, Barnsley L,
Oostendorp RAB et al (2003) Prognostic factors of whiplash-associated disorders: a system-
atic review of prospective cohort studies. Pain 104:303–322
21. Freeman MD, Croft AC, Rossignol AM (1998) Whiplash associated disorders: refining whip-
lash and its management. The Quebec Task Force. Spine 23:1043–1049
22. Stovner LJ (1996) The nosologic status of the whiplash syndrome: a critical review based on a
methodological approach. Spine 21:2735–2746
23. Jansen GB, Edlund C, Grane P, Hildingsson C, Karlberg M, Link H, Måwe U, Portala K,
Rydevik B, Sterner Y, Swedish Society of Medicine; Whiplash Commission Medical Task
Force (2008). Whiplash injuries: diagnosis and early management. The Swedish
Society of Medicine and the Whiplash Commission Medical Task Force. Eur Spine J
17 (Suppl 3):S355–S417
24. Eck JC, Hodges SD, Humphreys SC (2001) Whiplash: a review of a commonly misunderstood
injury. Am J Med 110:651–656
Functional Anatomy
3
C.L. Romanò, A. Mondini, S. Brambilla, and F. Ioppolo
The anterior faces of the cervical column is composed by a median portion made of
the overlapping of the vertebral bodies which include the intervertebral disks on top
of the bodies. This median portion is at first narrowed on the top (15 mm) and is
progressively broadened toward the bottom, reaching 25–30 mm at the last cervical
metamer.
The superior vertebral plate of the vertebral bodies that go from C3 to C7 ends
laterally with two osseous raised portions directed toward the top, called unciform
processes or uncus. These are included with the corresponding incisions on the lat-
eral inferior side of the above vertebral body, functionally behaving like true articu-
lations (Von Luschka articulations) that limit the lateral slant movement of the head.
Laterally, in correspondence of the top half of the vertebral bodies, the reliefs of
the transverse processes can be noticed, and they end laterally with their anterior
tuberculum. Of the latter, the C6 is called Chassaignac’s tuberculum and represents
an important surgical traceable point, since it is more neatly developed in respect to
the others (Fig. 3.1) [1, 2].
The intertransversal foramina are found in the middle of the transverse processes
and give way to the vertebral arteries which penetrate in most cases in C6, with its
veins, the vegetative nerve, and the rachis nerve.
C.L. Romanò
Center of Reconstructive Surgery and Osteoarticular Infection,
IRCCS “Galeazzi” Orthopedic Institute, via R. Galeazzi, 4,
20161 Milan, Italy
A. Mondini • S. Brambilla
“G. Pini” Orthopedic Institute, Via Rugabella 4,
20122 Milan, Italy
F. Ioppolo (*)
“Sapienza” University, Piazzale Aldo Moro 5,
00185 Rome, Italy

18 C.L. Romanò et al.
a b
Fig. 3.1 (a) Lateral view: vertebral artery (l) and rachis nerve (2) passing by the conjugate fora-
men. (b) Transversal section: intertansversal foramen (4). Anterior tuberculum (1); posterior tuber-
culum of the transverse process, peduncle (3); spinal channel (5); articular mass (6) with the
superior articular facet (7); uncus (8)
The posterior faces shows the reliefs of the spinal apophysis from C2 to C6 on
the median line, and both sides of the spinal apophysis extend to two osseous plates
that end on both sides: the first paramedian includes the series of the vertebral lami-
nae, lightly oblique externally, interrupted transversally by the narrow depression of
the interlaminar spaces. The second lateral side is formed by the overlapping of the
zygapophyseal articular processes and extends itself to the frontal plane for a
median width of 15 mm.
The external border of this side is easily found because it is blunt and sticks out
like a step [3].
A cavity separates the medial borders from the plane of the laminae: it represents
an important surgical traceable point because in front of it passes the vertebral artery
(Fig. 3.2).
Viewed in the lateral projection, the cervical column shows an anterior portion
formed by the alignment of the vertebral bodies, the intervertebral disks, two series
of reliefs of the transverse processes, and by a series of articular processes. The lat-
ter are piled on top of others to form the overall posterior articulations, character-
ized by an articular oblique interline, below and behind, forming an angular variation
of 30–50° from the horizontal line. This inclination makes the superior articular
process of each vertebra lay on a more anterior plane, with respect to the inferior
articulation of the same vertebra. The inferior articular process of a vertebra over-
laps on the superior articular process of the vertebra underneath (Fig. 3.3).
3 Functional Anatomy 19
a b
Fig. 3.2 (a) Posterior view: the articular mass has a mean width of 15 mm; a sulcus (dotted line),
well appreciable at surgery, separates the articular mass from the lamina; the white arrow shows
the projection of the vertebral artery. (b) Transversal section: the dotted line shows the projections
or the intertransversal foramen (asterisk) on the articular mass
a b
Fig. 3.3 (a) Lateral view: the articular mass are superimposed to form the plane of the posterior
zygapophyseal joints. (b) Detail of the zygapophyseal joint with their obliqueness ranges from 30
to 50° with respect to the horizontal plane
The transverse processes are inserted in front of the articular columns via the
connecting roots: an anterior one to the side of the vertebral body and the other one
posterior to the side of the articular columns, forming a cavity in front and out of the
Fig. 3.4 Conjugate foramen

(asterisk). (I) peduncle; (2)
articular mass; (3) transverse
process; (4) anterior
tuberculum; (5) posterior
tuberculum
conjugate foramen, through which the nerve roots abandon the rachis. The conjugate
foramen is delimited superiorly and inferiorly by the peduncles in the anterior part,
by the half inferior-posterior portion of the vertebral body, the lateral-posterior faces
of the intervertebral disk and the unciform processes and in the posterior portion by
the posterior articulation, reinforced on the anterior faces by the yellow ligament. It
lies on a mildly oblique plane 20° below the horizontal plane, in front and out about
30° of the frontal plane. It has median dimensions of 12 mm in height, 6 mm in
width, and from 6 to 8 mm in height (Fig. 3.4) [4, 5].
These dimensions are influenced by the movements of the rachis; in fact, the
conjugate foramina are open during flexion, lateral angulation, and rotation move-
ments on the opposite side. They close during extension, lateral angulation, and
rotation movement on the same side. The horizontal or transverse section includes
the vertebral cavity, anteriorly delimited by the laminae and yellow ligaments, later-
ally by the articular mass and by the peduncles. The vertebral foramen in the infe-
rior cervical rachis assumes a grossly triangular form with blunted angles; the
dimensions present great individual variability in the transverse and posterior diam-
eter. The figures at both ends of anthropometric studies vary from 19 to 29 mm in
the transverse sense from C3 to C7 and from 10 to 19 mm in the anteroposterior
sense from C3 to C7 [6].
The peduncles constitute osseous bridges that connect the vertebral bodies and the
articular mass; their distribution is along an oblique axis directed anteriorly and
medially with an angle of about 20°. On the cross section, they have an oval form with
an axis of 10 by 7 mm. Because of the small dimensions and the tight connection close
to the vertebral artery with the nerve root in the cervical rachis, the peduncles are not
considered to be good joining structures, rather the articular mass is preferred [7].
a b
Fig. 3.5 (a) Frontal view: anterior longitudinal ligament (J) and zygapophyseal joints (2).
(b) Posterior view: after removal of posterior arch: posterior longitudinal ligament (3)
The cervical metamers are joined together with the capsular ligament, essential
for vertebral stability [8, 9]. The anterior longitudinal ligament is a thin ribbonlike
translucent structure that without interruption extends itself on to the anterior
faces of the vertebral bodies. It is intimately connected to the vertebral limitants
and to the intervertebral disk, tightly adhering to the fibers of the annulus fibrosus
and to a lesser degree with the central portion of the vertebral body, resulting less
extent in width (Fig. 3.5). The annulus fibrosus appears tightly connected to the
cartilage of the vertebral plates in the peripheral part, practically in continuity
with the anterior and posterior longitudinal ligament [10, 11]. The posterior lon-
gitudinal ligament is a ribbonlike structure that extends itself along the posterior
faces of the vertebral bodies, connected to the limitants and to the disk but sepa-
rated from the central concave portion of the vertebral body. Its transverse exten-
sion becomes smaller from top to bottom, thereby increasing its width, which is
always greater than that of anterior longitudinal ligament (which reaches 3 mm).
It limits the flexion of the rachis and the movement of the vertebral bodies, pro-
tecting the spinal cord from herniations of the discal material in a median posi-
tion, while laterally leaving a breach for releasing the discal material in the
connecting channel.
The articular capsules are made of dense fibrous tissue tightly attached to the
osseous ends that extend horizontally for 5–7 mm. The capsular ligaments have
fibers that are orthogonal faces, and this allows some degree of controlled move-
ment. When the articular faces are in the neutral position, the fibers are more relaxed.
At the limit of their articular excursion, the fibers are tenser, due to their orientation,
limiting movement to a maximum of 3 mm with respect to the neutral position.
Even the orientation of the articular faces allows flexion of the column (a controlled
flexion) because it limits the outward anterior skid.
a b
Fig. 3.6 (a) Lateral view: yellow ligaments (J) and interspinal ligaments (2). (b) Bilateral view:
supraspinous ligaments connect two spinal apophyses crossing each other on the median line
Without the articular faces, the flexion is diminished, but an outward anterior
skid is seen, leading to an instability which is important to preserve in the posterior
approaches of the cervical column [12, 13].
The yellow ligaments represent the means of interlaminar union (Fig. 3.6) and
are tied from half of the inner faces of the above lamina to the topmost third of the
external faces of the lamina from below and included for the most part in the verte-
bral channel. Normally, the elasticity does not allow an introflexion, an impinge-
ment inside of the spinal channel during extension. Their hypertrophy, calcification,
or loss of elasticity due to degenerative factors can cause a dynamic stenosis with
compression of the spinal marrow. The interspinous ligaments are tied between two
spinal processes in an oblique and posterior direction; the supraspinous ligaments
are the continuation of the nuchal ligaments; they connect the apex of the spinal
apophysis crossing on the median line.
The cervical rachis includes nervous and vascular structures that are vitally
important, and since the latter are strictly bounded to the rachis, they can be
destroyed during traumatic events [14, 15].
The spinal cord is in the center of the vertebral body, enveloped by three mem-
branes (dura mater, pia mater, and arachnoid) that form the dural sac, which is sus-
pended by the dentate ligaments, bathed in the cephalorachidian fluid. The marrow
is an elastic structure that allows itself to adapt to various movements. During exten-
sion, it shortens itself and shows plicae on the surface. During flexion movements,
it elongates and its surface becomes smooth. The nerve roots take their origin from
the spinal cord with an anterior motor branch and the sensory posterior branch.
They go through a first and then a second extradural tract, starting from the opening
of the conjugation channel. The posterior root forms an ovoidal swelling within the
channel: the spinal ganglion. This forms an anastomosis with the anterior root,
forming the spinal nerve, which divides into its two anterior and posterior branches
at the exit from the conjugate channel forming the brachial plexus.
Dissection in vertebral and carotid arteries is uncommon, and the incidence of
cervical vascular dissection after whiplash trauma is not known even if widely
accepted that indirect neck trauma-like manipulations could be a cause of vertebral
dissection.
The vertebral artery [16] generally takes its origin from the subclavian artery and
penetrates into C6 and goes to C1, passing through the corresponding transverse
foramina. During its intrarachidial passage, it is enveloped by a sympathetic ner-
vous plexus and by a venous plexus. Both of these structures are strictly bonded to
the periosteum of the transverse foramina and are intimately attached to the nerve
roots at the cross-point outside of the conjugate channel [17]. The symptoms of
vertebral artery dissection are neck pain and signs of ischemia in the posterior cra-
nial fossa.
Another aspect to be considered about functional anatomy of the neck is the role
of venous vertebral plexus in drainage of cerebral venous blood [18].
The cerebrospinal venous system is a three-dimensional structure that is often
asymmetric and considerably represents a more variable pattern than the arterial
anatomy. The intracranial venous system is mainly composed of parenchymal veins
draining into the dural sinuses. The former can be subdivided into two systems:
1. The superficial (cortical) system reaches dural sinuses by cortical veins and
drains blood mainly from cortex and subcortical white matter
2. The deep cerebral venous system (DCVS) is composed by the internal cerebral
veins, the basal vein of Rosenthal, and the great cerebral vein of Galen and their
tributaries, and drains the deep white and gray matter surrounding the lateral and
third ventricles.
The cerebral veins collect blood into the dural sinuses and in turn redirected
toward the main extracranial venous outflow routes: the internal jugular veins (IJVs)
and the vertebral veins (VVs) system. The anatomical pathways of jugular drainage
are well established. The main jugular blood drainage pathway leads from the trans-
verse sinuses via the sigmoid sinuses into the IJVs, which meet the superior vena
cava via the brachiocephalic vein (Fig. 3.7) [19].
The VVs system is a freely communicating, valveless system present throughout
the entire spinal column and may be divided into an internal intraspinal part, the
epidural veins and an extraspinal paravertebral part. The system communicates with
the deep thoracic and lumbar veins, intercostal veins, azygous vein (AZ), and hemi-
azygos veins. The AZ represents the final collector of such an enormous plexus and
in turn drains into the superior vena cava, as well as into the inferior vena cava, via
the anastomosis of the hemiazygos veins with the left renal vein.
The blood leaves the brain by using the back propulsion of the residual arterial
pressure (vis a tergo), complemented by anterograde respiratory mechanisms (vis a
fronte). The latter consists of the thoracic pump increased venous outflow during
inspiration, thanks to increased thoracic negative pressure, which improves the
aspiration of blood toward the right atrium. In addition to vis a tergo and vis a
Sup.sagittal sinus(main
location of CSF return via
arachnoid granulations)
Inf.segittal sinus
Great cerebral v.
Sup. ophtalmic v.
Sphenoparietal sinus Straight sinus
Cavernous sinus
Sup. petrosal sinus Confluence
of the sinuses
Inf.petrosal sinus
Occipital sinus
Jugular loramen Transverse sinus
Sigmoid sinus
Int. jugular v.
Fig. 3.7 Venous drainage system from the brain to the neck. Internal jugulars vein are the main
way of cerebral venous blood in supine position, while when sitting or standing, they collapse and
the main way of cerebral drainage is through vertebral plexus (not represented) along all the spine
fronte, postural mechanisms play a main role in ensuring a correct cerebral venous
return. Several studies of healthy volunteers demonstrated that the pattern of cere-
bral venous drainage changes, even under physiological conditions, depending on
the body position:
• In the prone position, the outflow through the IJVs is favored
• The supine posture favors cerebral venous outflow through the IJVs
• Passing to the upright position transfers most of the encephalic drainage to
the VVs
It has been reported that flow is monodirectional in the IJVs/VVs. Flow is always
increased by the activation of the pump asking the subject to breath. Blood flow
velocity in the cervical veins is increased by activation of the thoracic pump.
Temporary outflow block can be seen in the cervical veins in healthy subjects, but
never reported in all the postural and respiratory conditions.
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Kinematics and Dynamics
of the Vehicle/Seat/Occupant System 4
Regarding Whiplash Injuries
P.L. Ardoino and F. Ioppolo
4.1 Introduction
Whiplash injuries continue to have significant societal cost; however, the mechanism
and location of whiplash injury is still under investigation. Predicting neck response
and injury resulting from motor vehicle accidents is essential to improving occupant
protection. Recently, the upper cervical spine ligaments, particularly the alar
ligament, have been identified as a potential whiplash injury location [1].
4.2 Accident Typology at the Origin of the Whiplash
From accident analysis, it has been noticed that neck injuries are mostly caused by
rear-end collisions: in a Dutch study conducted in the 1980s [2], neck injuries made
up 51.6 % of all the lesions found in the drivers of cars involved in rear-end collisions
(Table 4.1); in a Japanese study conducted at the beginning of the 1990s [3], the
neck injury percentage in rear-end collisions increased to 80 %.
A second characteristic of neck injuries is their low seriousness degree: the
abovementioned Japanese study [3] showed that during a rear-end collision, 93 %
of the injuries are classified as AIS 1 level according to the Abbreviated Injury Scale
[4]. As far as neck is concerned, in almost all cases, the AIS 1 level indicates a
P.L. Ardoino
FIAT Auto SpA, Technical Office,
Technical Coordination/Legal Safety, Orbassano (TO), Italy
F. Ioppolo (*)
00185 Rome, Italy

28 P.L. Ardoino and F. Ioppolo
Table 4.1 Distribution of injuries by body region for several collision types, driver only [1]
Lateral Total (including
Main group collisions Front to front Rear collisions other types)
1 Skull and brain 23.7 20.0 14.4 22.2
2 Face 11.2 21.1 7.2 16.1
3 Neck 4.4 3.7 51.6 6.9
4 Thorax 20.2 16.9 6.8 16.5
5 Abdomen 2.6 2.3 0.4 2.3
6 Back 2.4 1.3 4.0 2.4
7 Pelvis 5.0 1.3 0.4 2.0
8 Arms 16.0 13.6 7.2 14.2
9 Legs 14.5 19.8 6.0 17.3
Total (%) 100 100 100 100
100 %
31 % 42 % 6% 21 %
Fig. 4.1 Distribution of the rear accidents with injured occupants by impact type [4]
cervical rachis strain without any evidence of anatomical lesions. The same trend is
emphasized in a study conducted in Germany [5] on a sample of about 10,500 car
collisions.
With regard to the rear-end collision typology, in the abovementioned German
study [4], center and offset crashes make up about 73 % of all the rear-end collisions
(Fig. 4.1); only 27 % present an angled direction.
It is necessary to point out that in low-impact speed offset crashes, the off-
centering does not produce notable rotations in the hit vehicle, as it is regularly
noticed in damageability tests with off-center crashing barriers and above 20 km/h
crash speeds.
On the basis of what has been said above, we can conclude that, in almost all
cases, whiplash injuries happen in a low speed impact rear-end collision, in which
the speed variation takes place on the longitudinal axis of the vehicle.
4 Kinematics and Dynamics of the Vehicle/Seat/Occupant System 29
Fig. 4.2 Injury mechanism

in whiplash
4.3 Whiplash Injury Mechanism
In a rear-end collision, the chest is pushed forwards by the seatback; the burden on
the neck results from the strength of inertia that works through the center of gravity
of the head in a front-back direction; in this case, the neck injury mechanism is one
of hyperextension and tension (“traction” in mechanical terminology) of the cervi-
cal rachis (Fig. 4.2). It should be pointed out that not all hyperextension/tension
injury mechanisms are caused by whiplash.
Chronic radicular symptoms have been documented in whiplash patients, poten-
tially caused by cervical neural tissue compression during an automobile rear crash.
Simulated rear crashes with whiplash protection system (WHIPS) and active head
restraint (AHR) have been compared to those obtained with no head restraint (NHR)
with the aim to determine how whiplash may induce neural space narrowing of the
lower cervical spine [6, 7]. Average peak canal and foramen narrowing could not be
statistically differentiated between WHIPS, AHR, and NHR. While lower cervical
spine cord compression during a rear crash is unlikely in those with normal canal diam-
eters, it has been demonstrated [8] that foraminal kinematics is sufficient to compress
spinal ganglia and nerve roots. Disc strains are highest in the C4-C5-C6 segments.
4.4 Technical and Structural Limits
The technical norms now in force in Europe prescribe that the seatback must be
able to withstand the application of a static moment of 53 (m daN). Even though
from a theoretical point of view it is not possible to define a dynamic stress that
is equivalent to the static one, on the basis of experimental data and for normal
seats with 50 % male anthropometric characteristics, we can consider that such a
burden corresponds to the capacity to withstand the chest’s inertia load in a rear-
end collision between vehicles of equal mass with a closure speed of about
35 km/h.
Ignoring the retaining action of the headrest, we can deduce that speed varia-
tions of the vehicle higher than 18 km/h the seatback can rotate backwards absorb-
ing part of the chest kinetic energy; these phenomena in fact limit both the angle of
rotation of the head and the value of the extension moment.
The technical norms assure that the headrest withstands additional loadings
compared to the seatback.
We can therefore conclude that the crash that must be considered is a
rear-end one at AV < 18 km/h with a longitudinal movement of the passenger
compartment.
Review of whiplash injury mechanisms and effects of anti-whiplash systems,
including active head restraint (AHR) and Whiplash Protection System (WHIPS),
investigated whether seat design and biomechanical knowledge of proposed whip-
lash injury mechanisms translates to understanding outcomes of rear crash occu-
pants. In fact, in attempt to reduce whiplash injuries, some newer automobiles
incorporate anti-whiplash systems such as AHR or WHIPS. During a rear crash,
mechanically based systems activate by occupant momentum pressing into the
seatback, whereas electronically based systems activate using crash sensors and an
electronic control unit linked to the head restraint.
Biomechanical studies of simulated rear crashes have been performed using
human volunteers, mathematical models, crash dummies, whole cadavers, and
hybrid cadaveric/surrogate models. They indicated that AHR and WHIPS reduce
the potential for some whiplash injuries but did not completely eliminate the risk of
injury.
Epidemiological outcomes indicate reduced whiplash injury claims or subjective
complaints of crash-related neck pain between 43 and 75 % due to AHR and
between 21 and 49 % due to WHIPS as compared to conventional seats and head
restraints [9], concluding that energy-absorbing seats aim to reduce occupant loads
and accelerations, whereas AHRs aim to provide early head support to minimize
head and neck motions. Continued objective biomechanical and epidemiological
studies of anti-whiplash systems together with industry, governmental, and clinical
initiatives will ultimately lead to reduced whiplash injuries through improved pre-
vention strategies [10].
Some differences have been observed [11] regarding gender-based whiplash
effects in the dynamic response for the females with respects to the males in volun-
teer experiments. In fact the peak head acceleration in the posterior-anterior direc-
tion was higher and occurred earlier for the females than for the males. These
experiments could be used in developing and evaluating a female dummy model for
rear-impact safety assessment in order to design gender-specific protective
systems.
4.5 Phases of the Collision
A stereotypical kinematic and neuromuscular response has been observed in human

subjects exposed to rear-end impacts [6]. Combined with various models of injury,
these response data have been used to develop anti-whiplash seats that prevent
whiplash injury in many, but not all, individuals exposed to a rear-end crash.
Understanding of the occupant kinematics and neuromuscular responses, combined
with data from various seat-related interventions, have shown that differential
motion between the superior and inferior ends of the cervical spine is responsible
for many whiplash injuries. The number of whiplash injuries not prevented by cur-
rent anti-whiplash seats suggests that further work remains, possibly related to
designing seats that respond dynamically to the occupant and collision properties.
Neck muscles alter the head and neck kinematics during the interval in which injury
likely occurs, even in initially relaxed occupants. It remains unclear whether muscle
activation mitigates or exacerbates whiplash injury. If muscle activation mitigates
injury, then advance warning could be used to help occupant tense their muscles before
impact. Alternatively, if muscle activation exacerbates whiplash injury, then a loud
preimpact sound that uncouples the startle and postural components of the muscle
response could reduce peak muscle activation during a whiplash exposure [12, 13].
Generally speaking, rear-end collision is characterized by three different phases [14]:
• First phase: crash between the vehicles until the struck one assumes the speed
variation (AV) due to the impact conditions.
• Second phase: interaction between the seat and its occupant.
• Third phase: loadings on the occupant; the three phases surely are linked and
temporarily, partially overlapping.
4.5.1 First Phase
Regardless of the initial speed of the two vehicles, the struck one in this phase
assumes a speed variation that is a function of the masses of the vehicles, their clo-
sure speed, and the spring restitution coefficient; the analytic expression of the
speed variation of the vehicle that is hit is the following:
MA × MB
ΔVA= (VA - VB )(1 + e )
MA + MB
where:
A = struck vehicle
B = striking vehicle
V = speed at the impact
∆V = speed variation
M = mass
e = spring restitution coefficient
(VA − VB) = closure speed
Higher or lower stiffness of the vehicles brings a different degree of deformation

and therefore influences the duration of the collision and the values of average
acceleration, but does not modify the extent of the variation in speed.
4.5.2 Second Phase
The variations in motion of the hit vehicle are also those of the fastening of the
seat to the body shell; the seat, mostly the seatback, is the element through
which the occupant adapts its motion situation to the final one of the hit
vehicle.
In a rear impact, the seatback is the actual restraint system of the occupant, just
as the seatbelt is in a frontal impact.
It is important to point out that the fact of wearing the seat belt does not influence
the kinematics and the dynamics of the occupant during a lengthwise rear-end col-
lision; the only function of the seat belt in this particular case is to hold the occupant
once the crash is over.
Recently Viano et al. [15] analyzed matched rear sled tests with all belts to seat
(ABTS) and conventional seats from the same vehicle model to determine differ-
ences in BioRID IIg dummy responses. The BioRID IIg rear-impact dummy was
placed on ABTS or conventional seats and subjected to 10 m/h rear sled tests
using the Insurance Institute for Highway Safety (IIHS) whiplash assessment pro-
tocol. Measurements in the dummy included head and pelvis triaxial accelera-
tions, T1 and L1 biaxial accelerations, and upper and lower neck triaxial forces
and moments. High-speed video captured the dummy and seat kinematics during
seat loading and rebound into the lap-shoulder belts. Four vehicles were used with
conventional and ABTS seats in the same model. They were the 2007–2008
Chrysler Sebring, 2006 Ford F-150, 2005–2007 Saab 9–3, and 2006–2007 BMW
3 series.
Authors noticed that the upper neck tension was 44 % higher and the lower neck
extension moment was 102 % higher and that the Saab 9–3 responses were lower
than the 3 other vehicles for both the conventional and ABTS seats. There was less
rearward shear and extension of the neck in the Saab seats. In conclusion, the tests
show that ABTS seats involved significantly higher neck tensions, rearward shear
forces, and extension moments than matched conventional seats. Overall, ABTS
seats applied more load on the head and spine, had less control of neck kinematics,
and had higher risks for whiplash and more severe injury than conventional seats in
the same vehicle model.
Two characteristics of the seat influence the stress transfer from the vehicle to the
occupant: (1) the seat foam which cushions the stresses, filters, and further offsets
the small transversal and rotational movements of the vehicle; (2) the elasticity of
the seatback structure which obviously acts only in situations which do not exceed
the structural limits indicated before.
The relative head/headrest position plays a basic role in the extensional traction
movement of the neck and therefore in limiting the whiplash injuries.
Fig. 4.3 Rear-impact

simulation. Test configuration
80 80 Acceleration 180
Velocity
*
*
Displacement
Displacement (cm)
60 60 120
*
Velocity (km/n)
*
*
40 40 80
*
Accelaeration (g)
20 20 40
*
*
0 0 0
−20
−40
−60
0 40 80 120 160 200 240 260 320 360 400
Time (ms)
Fig. 4.4 Time histories of the passenger compartment
4.5.3 Third Phase
The human body is an articulated system of body segments which are submitted to
external loads, applied mainly through the seat, and they interact among themselves.
In order to analyze the stresses on the single-body segments, an experimental rear-
end collision test has been carried out on a crash simulator with the previously
described conditions (Fig. 4.3).
A 17 km/h variation in speed has been applied to the passenger compartment
with an acceleration curve corresponding to a rear-end collision with a rigid moving
barrier and, therefore, a particularly severe one (Fig. 4.4) segments.
Head accel.
3 chs
Neck load
3 chs
Head rotation
2 chs
Chest accel.
3 chs
Pelvis accel.
3 chs
Fig. 4.5 Hybrid III instrumentation
A Hybrid III dummy has been used in the front passenger position, provided with
the necessary instruments in order to obtain (Fig. 4.5): (1) the pelvis, chest, and
head accelerations; (2) the axial loads (compression and traction), the moments
(flexion and extension), and the shear force on the neck; (3) the rotation of the head
with regard to the basis of the neck.
Figure 4.6 shows the time histories (acceleration, velocity, displacement) of the
occupant’s pelvis, chest, and head in the direction of the applied forces that, in this
particular case, were horizontal-longitudinal.
80 80 BPX 160
60 60 120
Displacement (cm)
Acceleration (g)
Velocity (km/h)
40 40 80
20 20 40
0 0 0
80 80 160
TOPX
Acceleration (g)
Displacement (cm)
60 60 120
Velocity (km/h)
40 40 80
20 20 40
0 0 0
80 80 160
TPX
Displacement (cm)
120
Acceleration (g)
60 60
Velocity (km/h)
40 40 80
20 20 40
0 0 0
−20
−40
−60
0 40 80 120 160 200 240 280 320 360 400
Time (ms)
Fig. 4.6 Pelvis, chest, head time histories
It is necessary to point out that the head’s speed and displacement values above
130 ms do not correspond to the actual values of the speed and displacement com-
ponents along the X-axis, due to the rotation of the head.
It is therefore evident that the stresses on the three-body segments have different
values and are transmitted in different times.
80
60
Velocity (km/h)
40 Chest
20
Pelvis
0
−20
0 40 80 120 160 200 240 280 320 360 400
Times (ms)
Fig. 4.7 Pelvis, chest velocity vs time
The pelvis compared to the chest is subject to a stress that is shorter lasting, with
an average acceleration value which is higher, but it has a variation in speed which
does not exceed that of the vehicle (17 km/h); this means that, at pelvis level, the
seat and the seatback cushion the crash and do not elastically return energy to the
pelvis itself.
The duration of the stress on the chest is longer due to the spring restitution of
the seatback which, with a coefficient of about a 0.3, brings the chest’s variation in
speed to about 23 km/h.
Regarding the head, though we do not have the exact value of the variation in
speed along the horizontal-longitudinal axis, we have noticed a higher stress degree
in terms of both mean acceleration and variation in speed.
The head’s increase in speed variation compared to that of the chest is mainly
due to the neck’s spring restitution.
It should be noted that all the recorded acceleration values are at least one order
of magnitude below the human tolerance levels universally accepted in the biome-
chanic field for these body segments. The fact, which is also emphasized by the
accident analysis, that in rear-end collisions of this severity no pelvis, chest or head
injuries occur, does not alter the significance of the dynamic and kinematic trends
of the system which are the input conditions for the analysis of stresses on the neck.
The overlapping of the pelvis and chest speed curves (Fig. 4.7) shows how, in the
time interval between 80 and 200 ms, the variation in speed between chest and pel-
vis passes from about –l0 to +7 km/h.
The same behavior has been noticed between head and chest (Fig. 4.8). Regarding
stresses on the neck (moments and axial loads) (Fig. 4.9), we noticed a time corre-
spondence with the acceleration of the head; the same can be said for the rotation of
the head with regard to the basis of the neck. The head acceleration and speed
80
60
Head
Velocity (km/h)
40
20
−20
0 40 80 120 160 200 240 280 320 360 400
Times (ms)
Fig. 4.8 Chest, head velocity vs time
curves (Fig. 4.6) show, at about 80 ms, a small backward movement of the head, due
to the lever effect of the pelvis, chest, and seatback, to which a small bending
moment value corresponds (Fig. 4.9).
There is a question whether the standing or seated pelvis should be used in
Hybrid III dummy evaluations of seats and belt restraint systems in severe rear
impacts. Viano and Parenteu performed [12] sled tests in a belted standing and
seated Hybrid III dummy. The head, chest, and pelvis were instrumented with tri-
axial accelerometers and the upper and lower neck, thoracic spine, and lumbar spine
had transducers measuring triaxial loads and moments. Belt loads were measured.
In 40 km/h sled tests, the dummy motion and excursion were essentially similar
with the standing and seated pelvis. The similarities included the lap belt interaction
with the pelvis and the leg movement upward flexing the hip joint. Overall, similar
biomechanic and kinematic responses were found, including the pelvic accelera-
tion, spinal forces, and moments. For the lower speed tests at 10, 16, and 24 km/h,
the motion sequence was also similar with the two different pelvises, including the
upward movement of the legs as the seat was loaded and rebound kinematics. The
biomechanical responses were similar. The seated pelvis involves only a small por-
tion of the upper leg molded into the vinyl skin of the pelvis and does not limit leg
rotation at the hip joint. Furthermore, lap belt loads were minimal during the rear-
ward movement of the dummy. In conclusion, tests showed no significant difference
in occupant kinematics or biomechanical responses between the standing and seated
pelvis in rear sled tests.
By examining Figs. 4.6 and 4.9, the following can be noted:
• The chest starts its forward movement, pushed by the seatback, at about 50 ms.
• The rotation of the head starts at about 90 ms.
• The head’s center of gravity starts to shift forwards at about 120 ms.
40
Acceleration (g)
20
0
Head – resultant acceleration in the vertical longitudinal plane
40
Moment (N.m.)
Flexion
20
Extension
0
Neck – bending moment in the verticl longitudinal plane
Load (DAN)
100
Tension
Neck – axial load
20
Rotation (GR)
−20
−40
−60
Times (ms)
Head/chest – rotation in the vertical longitudinal plane
Fig. 4.9 Head and neck loadings
• The maximum stresses on head and neck occur at about 150 ms. Based on what
was mentioned above, it is clear that the neck – the link between chest and head
– is stressed in different ways during the crash (Fig. 4.10):
– Between 50 and 90 ms, the chest moves forwards and the head stays in its rest
position; the neck is essentially subject to small shear strains.
– Between 90 and 120 ms, the forward movement of the chest continues; the
head rotates due to the fact that the neck is subject to the application of an
extension moment.
Reference on
the ground +
+ + +
α
α
50 ms 90 ms 120 ms 150 ms
Fig. 4.10 Neck loadings and kinematics
– Between 120 and 150 ms, the head continues to turn and also moves forwards
pulled by the neck and pushed by the headrest. In this phase, the neck is sub-
ject to the largest stress of extension moment and traction force and whiplash
injuries occur.
Notice how, up to 200 ms (Fig. 4.6), and therefore after the largest stresses on the
neck have taken place, the occupant is in contact with and is meanwhile pushed
by the seatback; the seat belt up to now has not exercised any restraining action
and cannot therefore alter in any way the kinematics and dynamics of the
occupant.
On the basis of existing biomechanically based research [16], the following
occupant-related characteristics can influence the response of the cervical spine
during automotive rear impacts:
• Anatomical dimensions of the cervical spine
• Head-neck and cervical spine orientation at the time of impact
• Facet joint orientation
• Neck muscle size and orientation
The response of the cervical spine to rear impacts can be described using biome-
chanical concepts, but occupant-related factors can influence injury susceptibility
and biomechanically related researches outline the method by which those factors
affect the overall head-neck and cervical spine response in such a way.
4.6 Angled Rear-End Collisions
Regardless of the kind of rear-end collision, it is the seat which induces the stresses
on the occupant. In the case of mainly centered-angled rear-end collisions (Fig. 4.11),
which means angles not larger than 15–20°, the seat moves towards the occupant
C.G
C.G
Fig. 4.11 Centered-angled-rear collision; CG center of gravity
along the collision direction, and the stress components along the longitudinal axis
represent about 95 % of the total stress.
The neck injury mechanism is always an extension and tension one. In the worst
case, the movement occurs on a vertical plane tilted about 15–20° with regard to
the vertical longitudinal plane. In this case, due to the small size of the angle, the
human tolerance values in terms of extension moment and traction force could
slightly differ from those universally accepted in the biomechanic field for longitu-
dinal loads.
In the remaining kinds of offset-angled rear-end collisions, the rotation of the hit
vehicle dominates; the vehicle/occupant interaction does not take place solely
through the seat, and therefore the whiplash stress on the neck is unlikely to occur.
4.7 Out-of-Position Whiplash
Particular attention should be paid to the whiplash that occurs when the occupant is
out of position; for example, just think what the neck injury mechanism could be if
the stresses described above were applied to a head that initially is rotated around
its vertical axis of about 60°.
Very little knowledge is available on the human tolerance and on the biomechan-
ics of the rotated neck in the rear impact; nevertheless, an injured out-of-position
occupant should show an asymmetric lesion or symptomatology.
The necks of the current dummies do not allow us to study the injuries that could
result in these situations of asymmetric and compound stresses; in fact, their biofi-
delity is limited to the longitudinal vertical plane, and the neck structure is symmet-
ric with regard to any plane that passes through its vertical axis.
Conclusions
Automotive rear impacts are mechanical events and the response of the human
head-neck complex can be thought of in biomechanical terms.
Rear-impact collisions at low speed are a leading cause of economic costs

among motor vehicle accidents. Dummy tests focused on occupant position may
lead to development of specific tools aimed to reduce whiplash effects on the
head, the neck, and the trunk, both in drivers and passengers.
References
1. Ivancic PC, Xiao M (2011) Understanding whiplash injury and prevention mechanisms using
a human model of the neck. Accid Anal Prev 43(4):1392–1399
2. Van Kampem LTB (1993) Hoofdsteunen in personenauto’s. Institute for Road Safety Research
(SWOV), Leidschendam, Netherlands
3. Koshiro Ono (1993) Influences of the physical parameters on the risk to neck injuries in low
impact speed rear-end collisions. Proceedings of IRCOBI, Conference
4. Association for the Advancement of Automotive Medicine, Committee on Injury Scaling. The
Abbreviated Injury Scale—1990 Revision (AIS-90). Des Plains, IL: Association for the
Advancement of Automotive Medicine; 1990
5. Verband HUK (1994) Fahrzeugsicherheit 90. Verband HUK, Munchen
6. Siegmund GP (2011) What occupant kinematics and neuromuscular responses tell us about
whiplash injury. Spine 36(25 Suppl):S175–S179
7. Tencer AF, Mirza S, Bensel K (2002) Internal loads in the cervical spine during motor vehicle
rear-end impacts: the effect of acceleration and head-to-head restraint proximity. Spine
27(1):34–42
8. Ivancic PC (2012) Cervical neural space narrowing during simulated rear crashes with
anti-whiplash systems. Eur Spine J 21(5):879–886. Epub 2012 Jan 24
9. Panzer MB, Fice JB, Cronin DS (2011) Cervical spine response in frontal crash. Med Eng
Phys 33(9):1147–1159. Epub 2011
10. Fice JB, Cronin DS (2012) Investigation of whiplash injuries in the upper cervical spine using
a detailed neck model. J Biomech 45(6):1098–1102
11. Carlsson A, Linder A, Davidsson J, Hell W, Schick S, Svensson M (2011) Dynamic kinematic
responses of female volunteers in rear impacts and comparison to previous male volunteer
tests. Traffic Inj Prev 12(4):347–357
12. Viano DC, Parenteau CS (2011) BioRID dummy responses in matched ABTS and conventional
seat tests on the IIHS rear sled. Traffic Inj Prev 12(4):339–346
13. Ivancic PC (2011) Does knowledge of seat design and whiplash injury mechanisms translate
to understanding outcomes? Spine 36(25 Suppl):S187–S193
14. Arregui-Dalmases C, Pozo ED, Lessley D, Barrios JM, Nombela M, Cisneros O, De Miguel
JL, Seguí-Gómez M (2011) Driving position field study, differences with the whiplash protocol
and biomechanics experimental responses. Ann Adv Automot Med 55:71–79
15. Viano DC, Parenteau CS, Burnett R (2012) Influence of standing or seated pelvis on dummy
responses in rear impacts. Accid Anal Prev 45:423–431. Epub 2011 Nov 21
16. Stemper BD, Pintar FA, Rao RD (2011) The influence of morphology on cervical injury
characteristics. Spine 36(25 Suppl):S180–S186
Whiplash Lesions: Orthopedic
Considerations 5
E. Meani, S. Brambilla, A. Mondini, C.L. Romanò,
and F. Ioppolo
5.1 Introduction
Whiplash usually stands for a syndrome characterized by a soft tissue lesion of the
neck (muscles, ligaments, capsules, intervertebral disk, spinal marrow, nerve roots,
veins and arteries, sympathetic system).
Normally though, this term is used in a broader way to define the majority of
traumatic events that involve the cervical rachis following street accidents. In this
context, whiplash does not represent a clinical syndrome, but rather comprises a
group of pathological entities that are extremely different in their entity, prognosis,
and treatment.
5.2 Clinical Course
In an acute phase right after the trauma, the symptomatology is characterized by

pain in the cervical and occipital areas, with the addition of the scapular girdle and
the dorsal region; the tendency is to reach a peak in the following hours and days
E. Meani • C.L. Romanò

Center of Reconstructive Surgery and Osteoarticular Infection,
IRCCS “Galeazzi” Orthopedic Institute, Via R. Galeazzi 4,
20161 Milan, Italy
S. Brambilla • A. Mondini
“G. Pini” Orthopedic Institute,
Via Rugabella 4, 20122 Milan, Italy
F. Ioppolo (*)
00185 Rome, Italy

44 E. Meani et al.
with establishment of a muscular contracture of the paravertebral muscles (trape-

zius muscle and the long muscles of the back).
These symptoms are totally aspecific and are mostly all present in the traumatic
affections of the rachis; there is no relationship between the extent of the symptom-
atology and the gravity of the lesions [1].
Normally, in the acute phase, no signs of involvement of the myeloradicular
structures of the rachis are present. If these signs were evident, they indicate a lesion
of the soft tissues and the osteoarticular structures.
The symptomatic pain can completely resolve itself in a variable period of time
from the traumatic event or it can become chronic. The clinical course is worsened
with symptoms such as headache, nausea, tinnitus, lack of concentration, photopho-
bia, retro-orbital pain, anxiety, depression, easy irritability, sleep disturbances, and
dysesthesias of the upper limbs. Carrol et al. [2] in a prospective cohort study
design, through a self-reported scale which investigated pain, depression, anxiety,
fear, anger, and frustration, showed that pain-related frustration was the most
intense. Only 3 % of the cohort reported having no pain-related frustration, and 4 %
reported no pain-related anxiety. Their findings suggest that it may be beneficial for
health care providers to address emotional status related to pain in the first few
weeks after a whiplash injury.
Neck pain is determined by contracture of the paravertebral cervical muscles and
is accompanied by a limitation of the articular excursion; the most involved muscles
(sternocleidomastoid, scalene, trapezius, long neck muscles) can determine lesions
that go from simple stretching to rupture with the formation of intrafascicular hema-
tomas. The same stretching lesions can also involve the anterior and posterior long
ligaments. Less frequent are cleavages and lacerations of the annulus fibrosus, sepa-
ration of the somatic limiting of the cartilaginous plate, and lesions that can predis-
pose to discal degeneration, which contributes to prolonging the symptomatic pain.
With some frequency, pain in the interscapular and high dorsal regions has been
reported, expression of the myofascial lesions of the trapezius, rhomboid, levator of
the scapular muscles, and large dentate muscle.
If the brachial pain and paresthesias are not tied to an irritative-compressive fac-
tor of the nerve roots (discal protrusion, stenosis of the conjugate channel, compres-
sion of a fractured articular apophysis), they do not generally present with a precise
metameric distribution and remain difficult to interpret, even if they have been indi-
cated as a possible cause of lesions associated with the brachial plexus or with a
thoracic outlet syndrome.
Widespread hyperalgesia in chronic whiplash-associated disorders have been
showed by Lemming et al. [3] that investigated deep tissue pain hyperalgesia in
women using computerized cuff pressure algometry and hypertonic saline infusion.
They demonstrated a widespread hyperalgesia with facilitation of temporal summa-
tion outside the primary pain area, suggesting involvement of central sensitization.
Headache in the occipital area is a common symptom; generally, it is due to a
painful muscular spasm of the semispinal muscles and rectus muscles of the head
and neck, or splenius muscle, or to stretching or laceration of the nuchal ligaments
[4]. Often, in association, there is a neuralgia of Arnold’s large occipital nerve.
5 Whiplash Lesions: Orthopedic Considerations 45
The retro-orbital pain and the reading fatigue that are often included in the com-
plaints of patients with whiplash injuries could be tied to a proprioception problem
of the paravertebral muscles, with major involvement of the intrinsic oculomotor
system.
5.3 Diagnosis
Due to the aspecificity of the clinical picture, it is necessary to recur to a radio-

graphic examination in a patient suffering from traumatic injury of the spine. Recent
studies evidenced morphological changes (atrophy and fatty degeneration) of neck
muscles in whiplash-associated disorders (WAD) highlighted emerging evidence
for the pathophysiological mechanisms behind muscle degeneration and their
potential role in the transition from acute to chronic pain [5].
Magnetic resonance imaging (MRI) can be regarded as the gold standard for
muscle imaging. There is emerging evidence to highlight in vivo features of neck
muscle degeneration in patients with chronic WAD and the temporal development
of such acute changes after trauma. However, the precise underlying mechanisms
for such changes and their influence on functional recovery after whiplash remain
largely unknown, even if current evidence from structural MRI-based studies dem-
onstrates the widespread presence of fatty infiltrates in neck muscles of patients
with chronic whiplash. Such findings have not shown to feature in patients with
chronic insidious onset neck pain, suggesting traumatic factors play a role in their
development. Recent studies have revealed that the muscle fatty infiltrates manifest
soon after whiplash but only in those with higher pain, disability, and symptoms of
post-traumatic stress disorder. The possibility that such muscle changes are associ-
ated with a more severe injury, including poor functional recovery, remains the
focus of current research efforts.
Under an orthopedic point of view, the first step is X-ray diagnosis, at least for
the acute cases in emergency room; it should include, apart from the classical fron-
tal and lateral projections, the oblique and transoral projections, all easily perform-
able exams in an emergency room. Fundamentally important is good execution and
interpretation of the above exams: the lateral projection assesses alignment of the
vertebral bodies (anterior and posterior somatic lines), the normal orientation of the
articular faces, and the absence of fanning of the spinal apophysis [6].
The anterior-posterior projection is used to evaluate the correct alignment of the
spinal apophysis, the peduncles, and the normal position of the vertebral bodies and
the articular mass (Fig. 5.1).
In case of abnormal position of the vertebrae in these two standard projections,
it is good to recur to the oblique projections, especially in cases that too often are
thought to be partial dislocations. The oblique projections can better point out the
posterior articular structures, the peduncles, and the normal conformation and
dimension of the conjugate foramina (Fig. 5.2) [7, 8].
Furthermore, it is necessary to remember that at the moment of the trauma, an
extensive antalgic muscular contraction can hide a grave lesion of the capsular,
46 E. Meani et al.
a b
Fig. 5.1 (a) Lateral view: dashed line shows the normal position of the vertebral bodies (1) and
correct alignment of the peduncles and articulator mass (2). (b) Anteroposterior view: dashed line
shows the correct alignment of the spinal apophysis and normal position of vertebral bodies
Fig. 5.2 Oblique view

Fig. 5.3 Severe whiplash trauma
disk, ligament structures (severe sprain). However, this will eventually become clear
with execution of radiographs in the lateral projection in maximal flexion and exten-
sion positions [9].
Pressure pain threshold (PPT) could provide additional prognostic ability to pre-
dict short-term outcomes in people with acute whiplash, but it has yet to be explored
in people with acute (of less than 30 days in duration) whiplash-associated disorder.
PPT measured at a site distal to the injury is the most parsimonious predictor of
short-term neck-related disability score, and it represents promising addition to
assessment of traumatic neck pain even if neither age nor PPT at the local site is able
to explain significant variance of results [10].
Dynamic radiographs will evaluate signs of vertebral in stability that consist [11]
of (1) anterolisthesis of a vertebral body with respect to the one underneath and
>3 mm, (2) loss of contact and alignment of the zygapophyseal articular surfaces
>50 %, (3) increase of the interspinal distance with respect to the upper or lower
metamers (fanning), (4) elective discal kyphosis, and(5) angulation of the posterior
somatic wall ~15° (Fig. 5.3).
The simultaneous presence of “at least three of” the above radiographic signs
suggests a severe sprain, an instable lesion that implies a surgical type of treatment.
A partial dislocation or a lesion that in the lateral projection points out a mild ante-
rior sliding of a vertebral body with respect to the one underneath cannot be underes-
timated, because it is often tied to an unilateral lesion (fracture or dislocation of a
articular apophysis, pillar fracture); the rotation type implies a mild skid in an antero-
posterior sense. In this case, even if the standard projection can point out a correct
48 E. Meani et al.
Fig. 5.4 In the lateral view, the articular mass is usually shown as one image as the articular
apophyses are superimposed on each other. In this case of unilateral fracture-dislocation of C6, the
articular mass present a double profile due to the rotational component. The arrow shows the mild
shift typical for unilateral lesions
diagnosis (loss of an alignment of the spinal apophysis in the frontal projection;

doubling of the articular apophysis silhouette in the lateral projection), the oblique
projections eliminate all doubts and indicate correct treatment (Fig. 5.4) [12, 13].
In the unilateral fractures, there is an eventual decomposition of the articular
apophysis and its rime (frequently the top ones), or in case of dislocation, there is a
stenosis in the conjugate foramina and loss of the normal alignment of the zyg-
apophyseal articular surfaces (Fig. 5.5).
In the pillar fracture of the facial mass, the characteristic sign is the horizontal-
ization of the articular mass This happens because this peculiar cervical rachis
lesion is characterized by two rimes of fracture: the anterior one in the peduncle and
the posterior one within the laminae that isolate the articular mass, which is com-
pletely torn off and can rotate downward and forward, losing its normal oblique
position in the lateral projection (Fig. 5.6).
The CT scan in this case will better evidence the two rimes of fracture, while in
unilateral lesions it will confirm the diagnosis and show other lesions such as lamina
fractures, not well distinguished with traditional radiology (Fig. 5.7) [9]. Magnetic
resonance imaging (MRI) is especially indicated in patients who show persisting
algesic symptomatology with radiation to the upper limb and with paresthesias,
even if the metameric distribution is not precise.
a b
Fig. 5.5 (a) Unilateral fracture-dislocation C6–C7. The arrow shows the absence of normal align-
ment of zygapophyseal articular surfaces. The asterisks show the altered relationship between uncus
and the semilunar facet. (b) The CT scan points out the stenosis of the conjugate channel (arrow)
a b
Fig. 5.6 Fracture of the articular mass of C5. (a) Lateral view, showing a mild sliding of C5 over
C6. (b) Oblique view: the articular mass of C5 (asterisk) is anteriorly and downward rotated,
narrowing the conjugate foramen of C4–C5
50 E. Meani et al.
a b
Fig. 5.7 (a) Fracture of the articular mass. The CT scan shows the fracture of the peduncle (1) and
a second fracture line at the junction between the lamina and the articular mass (2). (b) In unilateral
lesions the CT scan can show associated lesions, like fracture of the lamina (1) and (2) of the
transverse process
MRI allows to demonstrate rupture of the anterior longitudinal ligament, osteochon-

dral detachments of the vertebral plate, cleavages of the annulus fibrosus, separation of
the intervertebral disk from the vertebral plate, and, frequently, discal protrusion.
Radiological findings associated with poor recovery following whiplash injury
remain elusive [14]. Muscle fatty infiltrates in the cervical extensors occur soon
following whiplash injury and suggest the possibility for the occurrence of a more
severe injury with subsequent post-traumatic stress disorders (PSTD) in patients
with persistent symptoms. MFI in the cervical extensors on MRI in patients with
chronic pain have been observed. According to Elliot et al. (2011) [15], MFI values
increased in moderate/severe group and were significantly higher in comparison to
the recovered and mild groups at 3 and 6 months. They did not find differences in
MFI values between the mild and recovered groups. Initial severity of PTSD symp-
toms mediated the relationship between pain intensity and MFI at 6 months.
5.4 Treatment
The initial phase of treatment of mild distortional forms of whiplash involves immobili-
zation with a rigid or Philadelphia-type collar for a period of time not less than 2 weeks.
From a pharmacological point of view, the patient will benefit from the admin-
istration of analgesics (NSAIDs), myorelaxants (more efficient if with central
action), and anti-vertigo drugs. With the removal of the orthopedic support, it
will be important to restore muscular tone to guarantee correct posture and kine-
matics of the cervical column: this is possible with physical training and
stretching.
There are few diagnostic tools for chronic musculoskeletal pain as structural
imaging methods seldom reveal pathological alterations. Linnman et al. (2012) [16]
visualized inflammatory processes in the neck region by means of positron-emission
tomography using the tracer C-D-deprenyl, a potential marker for inflammation in
22 patients with enduring pain after a rear-impact car accident (whiplash-associated
disorder grade II). They showed that patients, with respect to controls, displayed
significantly elevated tracer uptake in the neck, particularly in regions around the
spinous process of the second cervical vertebra, suggesting that whiplash patients
have signs of local persistent peripheral tissue inflammation, which may potentially
serve as a diagnostic biomarker.
It is useful to combine gymnastics with physiokinetic therapy, massage therapy,
TENS, and ultrasound, which all have analgesic action. Vertebral manipulation is
still controversial, particularly in elderly subjects in whom degenerative alterations
of the cervical rachis are present, due to the risk of permanent neurologic lesions.
In a later phase, the persisting algesic symptomatology in some patients can be
relieved by the infiltration of steroid compounds in the posterior articular facies,
possibly associated with local anesthetics.
Noninvasive treatment is normally undertaken in the true forms of whiplash or in
mild traumatic sprain (mentioned earlier). This includes most of the traumatic
events occurring in the cervical column anel, as mentioned above, can lead to loss
of rachis stability for osteo, disc, capsular, and ligament lesions, immediately or
after the initial trauma. Instability, meaning the loss of the normal vertebral struc-
ture, needs more substantial treatment, such as more extreme immobilization with,
e.g., the halo-vest for lesions in which the instability is exclusively or almost all
osseous (thus temporaneous), with the possibility of treatment by consolidation of
the fracture (pillar fracture without radicular lesion).
Surgical treatment is suggested for permanent instable forms (severe sprain,
decomposition articular fractures, unilateral dislocations, pillar fracture with severe
decomposition, and simultaneous reticular lesion), with protrusions and discal her-
nias with medullar radicular lesion.
The surgical options include intersomatic discectomy, arthrodesis performed
anteriorly by Smith and Robinson’s technique, possibly associated with a plaque
screwed on to the upper and lower vertebral bodies, and posterior osteosynthesis by
screwing together the articular mass, perhaps associated with arthrodesis (Figs. 5.8
and 5.9).
5.5 Prognosis
Prognosis of whiplash injury has been found to be related to a number of sociode-

mographic, treatment, and clinical factors. Dufton et al. (2012) [14] attempted to
identify prognostic factors for delayed recovery using a validated and reliable
52 E. Meani et al.
a b
Fig. 5.8 Intersomatic arthrodesis performed by an anterior approach: at one level (a) or two levels
(b) with different osteosynthesis devices. Asterisks indicate the autologous bone graft
Fig. 5.9 Osteosynthesis with

plate of the articular mass via
a posterior approach
measure of recovery in a retrospective review of a large database from a national

network of physiotherapy and rehabilitation service providers in Canada.
In a group of 5,581 individuals injured in motor vehicle collisions, they demon-
strated positive outcomes to be proportionally fewer in the chronic cohort (52.1 %)
relative to the early chronic (61.4 %), which was in turn lower than the acute cohort
(72.3 %). Furthermore, individuals presenting with chronic pain were more likely to:
1. Be female
2. Be present with lower limb pain or nonorganic signs
3. Have returned to work
4. Have retained a lawyer or
5. have undergone previous spinal surgery
They were less likely to:
1. Be present with neck or mid-back pain
2. Live in Ontario or Nova Scotia
3. Have modified duties upon return to work
Generally speaking, recovery in whiplash-associated disorder appears to be mul-
tifactorial with both medical and noninjury-related factors influencing outcome.
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tent musculoskeletal inflammation. PLoS One 6(4):e19182
Neurology of Whiplash
6
G. Meola, E. Bugiardini, and E. Scelzo
6.1 Introduction
Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck

which may result mainly from rear-end or side-impact motor vehicle collisions but
also from diving or other mishaps [1]. Whiplash-associated disorder (WAD) is gen-
erally considered to be a soft tissue injury of the neck with symptoms such as neck
pain and stiffness, headaches, cognitive and psychiatric disorders, dizziness, visual
symptoms, paresthesias, and weakness. It is estimated that the incidence of whip-
lash injury is approximately 4 per 1,000 persons [2]. Although many persons
involved in whiplash injuries recover quickly, between 4 and 42 % of patients report
symptoms several years later [2, 3]. According to Quebec Task Force, late whiplash
syndrome has been defined by the symptoms persistence for more than 6 months
after the injury. Patients with neurological symptoms caused by whiplash syndrome
are frequently referred to neurologists in everyday clinical practice.
The relevance of neurological signs in whiplash syndrome is highlighted by their
role on determining the severity of the disease in Quebec Task Force classification
of WAD (see Chap. 24).
6.2 Clinical Presentation
Clinical presentation of patients affected by whiplash syndrome may include differ-

ent symptoms and signs involving both central and peripheral nervous system (see
Table 6.1). Although it is one of the most relevant symptoms of whiplash syndrome,
G. Meola (*) • E. Bugiardini • E. Scelzo

Department of Neurology,
University of Milan, IRCCS Policlinico San Donato Milanese,
Via Morandi 30, San Donato Milanese,
Milan 20097, Italy
e-mail: giovanni.meola@unimi.it

56 G. Meola et al.
Table 6.1 Neurological symptoms after whiplash injury

Headaches Migraine-type headache
Tension-type headache
Cervicogenic-type headache
Temporomandibular joint derangement
Greater occipital neuralgia
Third occipital headache
Cognitive and psychological Memory, attention, or concentration impairment
symptoms Sleep disturbance
Psychiatric disorders: anxiety, depression, phobic travel,
anxiety, and post-traumatic stress disorder
Dizziness Vestibular dysfunction
Cervical origin
Brainstem dysfunction
Visual symptoms Blurred vision
Reduced visual field
Photophobia
Disordered fusion
Reading and driving difficulties
Reduced accommodation
Paresthesias Trigger points
Brachial plexopathy
Cervical radiculopathy
Spinal cord compression
Weakness Brachial plexopathy
Cervical radiculopathy
Spinal cord compression
Rare symptoms Torticollis
Tremor
Transient global amnesia
Hypoglossal nerve palsy
Superior laryngeal nerve paralysis
Cervical epidural hematoma
Brainstem infarct
Internal carotid and vertebral artery dissection
Symptomatic Chiari malformation
neck pain will not be discussed because in the majority of cases, it is thought to be
due to a myofascial injury (of orthopedic pertinence).
6.3 Headaches
The incidence of headache in whiplash patients varies widely depending on meth-

odologies utilized in the past studies. Unspecific headache in acute stage seems to
be present in 50 % to more than 75 % of cases, while in 25–33 % of the cases,
symptoms become chronic [4].
6 Neurology of Whiplash 57
The origin of whiplash headache is probably multifactorial. In the second edition

of the International Classification of Headache Disorders (2004) [5], whiplash
headache has been classified in two categories: acute and chronic form. To fulfil the
diagnostic criteria, headache, at the time accompanied by neck pain, must develop
within 7 days after a whiplash injury. In the acute form, headache resolves within
3 months after whiplash injury, while in chronic form it persists longer. Diagnostic
criteria do not specify typical characteristics of headache thus leading to question
their application in clinical practice [6]. In previous studies, whiplash headache has
been described as migraine-, tension-type headache, or cervicogenic headache [4].
A recent analysis showed that the headache after whiplash may represent a primary
headache (mostly migraine- or tension-type headache) elicited by the stress of the
situation [7].
Besides the unspecific headaches reported before, other factors as temporoman-
dibular joint derangement [8], greater occipital neuralgia [9], and third occipital
headache may contribute to the development of cephalalgia. Greater occipital neu-
ralgia may be a consequence of whiplash injury especially in patients with anatomic
entrapment of the nerve. Indeed in cases in which greater occipital nerve pass
through the trapezius muscle, it may be damaged during neck flexion and extension
typical of whiplash injury [9]. Third occipital headache was a condition investigated
by Bogduk that consisted of referred headache caused by a C2–C3 zygapophyseal
joint injury [10]. C2–C3 zygapophyseal joint is innervated by third occipital nerve
whose afferent fibers converge with trigeminal afferents in spinal cord creating a
neuroanatomical basis of referral pain to the head [10]. Using third occipital nerve
block to diagnose this form of headache, Lord et al. [11] found a prevalence varying
from 38 to 58 % in patients with headache post-whiplash.
6.4 Cognitive and Psychological Symptoms
Cognitive symptoms are a frequent complaint of patients with whiplash. In different

studies, the prevalence of cognitive disturbances such as memory, attention, and
concentration impairment was nearly 50 % [12, 13].
Previous neuropsychological examinations have found a deficit in attention tests
[14] that was supposed to depend on the emotional dysfunction and the distracting
effect of pain. Radanov [15] supports the concept that psychological and cognitive
problems of patients with common whiplash are mainly related to somatic symp-
toms. Other works do not confirm the presence of deficit in neuropsychological test
in patients with cognitive symptoms [13]. They suppose that cognitive problems
appear to be indicators of heightened somatic vigilance rather than indicators of
actual neuropsychological deficits. Additionally, somatization and inadequate cop-
ing may contribute to subjective complaints and poor performances in these patients
[16]. Moreover, a recent study on MRI-based brain volumetry did not find any alter-
ation in chronic whiplash patients [17]. Studies based on SPECT, PET, and func-
tional MRI showed controversial results on the presence of specific brain alterations
in whiplash [18, 19].
58 G. Meola et al.
6.4.1 Sleep Disturbance
Sleep disturbances are common in patients after a whiplash injury ranging from 39
to 87 % of cases [20, 21]. Prevalence is higher immediately after the injury and
patients’ complaint falls significantly thereafter [21]. Sleep monitoring by actigraph
failed to demonstrate significant alterations in sleep latency, sleep duration, number
of arousals, or sleep efficiency. Otherwise, their subjective impression of sleep qual-
ity was significantly lower compared to controls [22].
Available data cannot exclude the presence of subtle, but clinically important,
sleep disturbances demonstrable by polysomnography. Another recent work found
an association between sleep disturbances and the intensity of pain [23] that is sug-
gested to be one of the most relevant factors in determining sleep alteration.
6.4.2 Psychiatric Disorders
Mental symptoms after a whiplash injury are common. Psychological disorders

have been found with a prevalence of 37 % at 3 months, 35 % at 1 year, and 35 %
at 3 years after whiplash injury [24]. The alterations more frequently individuated
are anxiety, depression, phobic travel anxiety, and post-traumatic stress disorder
[24]. Reported psychiatric disorders are not specific of whiplash injury but are com-
parable to those following other types of injury (i.e., road traffic agents) [24]. The
increased prevalence of anxiety disorders and depression is also supposed to be
related to chronic pain suggesting that whiplash traumas should be considered in the
same way as other chronic pain syndromes [25]. An interesting point of view is
what emerges from the work of Mykletun et al. [26] which hypothesizes a reverse
causality between whiplash and symptoms of anxiety and depression. Indeed, they
found a higher incidence of chronic whiplash syndrome in patients already affected
by anxiety and depression supporting that chronic whiplash may represent to some
degree a functional disorder. The importance of psychological factors on the devel-
opment of late whiplash syndrome is supported by recent evidences about the asso-
ciation between specific personality traits and the chronicization of symptoms [16].
6.5 Dizziness
Dizziness is a frequent complaint in patients with whiplash syndrome, reaching the

70 % of patients with chronic symptoms [27]. The dizziness may origin from an
alteration of different systems that may be involved in whiplash-associated disor-
der. Direct dysfunction of the vestibular apparatus, such as benign paroxysmal posi-
tional vertigo (BPPV), may lead to true vertigo in whiplash patients. In a recent
work of Dispenza et al. [28], it was found that 33.9 % of patients with whiplash
injury present BPPV and it was underlined the importance of a correct individuation
of these patients to perform a specific therapy. Dizziness of cervical origin is another
frequent cause of dizziness in whiplash patients. Direct trauma on the neck may
modify muscle spindle sensitivity leading to an alteration of cervical afferent input

to the postural control system and a secondary impairment of the vestibular and
visual system [29]. Vertebrobasilar artery insufficiency has been reported as a pos-
sible cause of dizziness, but more studies are needed to better define its role in
whiplash syndrome [30]. Another cause of dizziness of cervical origin was that
proposed by Barré and Lieou in 1928 [31] (posterior cervical sympathetic syn-
drome, Barré-Lieou syndrome). It was supposed that posterior circulation (includ-
ing circulation of inner ear) was innervated by sympathetic nerve emerging from
cervical roots. The cervical roots compression led to sympathetic irritation and con-
sequently vasoconstriction and ischemia of inner ear. This theory is not widely
accepted, and no recent papers supporting it have been published [32].
In conclusion, a brainstem dysfunction due to movement of brain within the
skull may be a further cause of dizziness through an alteration of the inhibitory
effect on the vestibular nuclei [33].
6.6 Visual Symptoms
Visual and ocular disturbances in whiplash syndrome have been widely reported in
literature. They include not only disorders complained by patients as blurred vision,
reduced visual field, photophobia, disordered fusion [29, 34], reading and driving
difficulties [35], or reduced accommodation [29, 34] but also ocular alterations
found in both symptomatic and asymptomatic patients (oculomotor system deficits,
disturbances in smooth pursuit, eye movement with neck torsion, or saccadic eye
movement) [29, 34, 36]. Most of the visual disturbances described in whiplash are
thought to reflect an alteration in central connections between the eyes and the cer-
vical afferents. Other visual symptoms may depend on injury to the brainstem or to
higher centers in the central nervous system [37]. A significant reduction in the
amplitude of accommodation was found in whiplash patients reporting visual dis-
turbances [38]. Deficient accommodation has been attributed to an interruption or
stimulation of the sympathetic pathway; to vascular disturbances of the vertebral,
basilar, or internal carotid artery; or to lesions of the midbrain in the area of the third
nerve nucleus [38]. Oculomotor system deficits have also been reported and seem
to be mostly related to cervical afferent disturbances [39]; they are generally mild
and are characterized by a good prognosis [40].
6.7 Paresthesias
Numerous clinical studies have documented paresthesias of neck, shoulders, upper

back, and arms in whiplash patients. Norris and Watt found that the incidence of
paresthesias acutely complained by patients ranged from 33 to 100 % depending on
the presence of neurological abnormalities and the evidence of neurological loss.
Symptoms tend to persist in a variable number of subjects after 6 months [41].
Paresthesias in the upper extremities can be caused by myofascial injuries with
60 G. Meola et al.
trigger points, by brachial plexopathy including thoracic outlet syndrome, and less
often by cervical radiculopathy and spinal cord compression. Sometimes trigger
points localized in several neck and trunk muscles can cause referred paresthesias
in the upper extremities [42]. Whiplash injuries are a common cause of thoracic
outlet syndrome (TOS) [43]. Whiplash injury would most likely affect a narrowing
of the scalene triangle by spasm of the scalene muscles, but may also cause a reduc-
tion of the costoclavicular space by an elevation of the first rib, again secondary to
continuous contraction of the scalene [44]. Some authors hypothesize that many
patients with harm symptoms persisting more than some months after the injury
might be affected by a neurogenic type of TOS caused directly by the trauma or by
a secondary TOS related to cervical disc injury. The latter type of TOS is supposed
to be caused by an alteration of anterior or posterior scalene muscles secondary to
the involvement of the roots they are innervated by (C5–C7) [45]. Additionally,
despite rarely, whiplash injuries can induce other brachial plexus lesions such as
long thoracic and spinal accessory nerve injuries [46–48]. Paresthesias may also be
associated with nerve root, ganglion, and spinal cord compression. During rear
impact, the intervertebral levels of the lower cervical spine can undergo hyperexten-
sion, which may cause reduction in the cervical foraminal area and in canal diame-
ter leading to nerve root, ganglion, and spinal cord damage [2, 49]. Several authors
have found a strong association between radiculopathy and foraminal spondylosis
preceding whiplash injury. Recent studies showed that rear impact may cause gan-
glion compression also in nonspondylotic foramen mainly at C5–C6 and C6–C7
levels but that the injury risk greatly increases in patients with spondylotic foramen
involving also C3–C4 and C4–C5 levels [49, 50]. Repeated ganglion or nerve root
compression caused by an increased joint laxity or instability induced by ligamen-
tous injury has been supposed to be one of the most important risk factors for chro-
nicization of radicular symptoms. This risk is exacerbated in individuals with
foraminal spondylosis due to smaller bony foraminal dimensions [49]. Central cord
injury without vertebral fractures is uncommon in whiplash syndrome. Although
recent evidences have revealed that spinal cord injury is even possible in subjects
with normal cervical canal, almost all cases are reported in patients with cervical
stenosis and only after wide neck extension [51, 52].
6.8 Weakness
Complaints of upper extremity and neck weakness are common after whiplash inju-
ries. Weakness may be caused by brachial plexopathy, cervical radiculopathy, and
spinal cord compression with mechanisms similar to those described for paresthe-
sias. Weakness is reported by patients even when there is no evidence of nervous
system involvement. Some studies reported very low cervical strength scores in
both acute and chronic whiplash patients [53, 54]. Prushansky et al. [54] found that
cervical strength is reduced by about 80 and 90 % in women and men, respectively,
compared to controls especially in extension patterns of movement. Although there
is no consensus about it, recent studies have found no changes of cervical muscle
volumes 6 months after whiplash injury and no consistent correlation of muscle

volumes with clinical variables [55]. In the absence of severe atrophy or neurologi-
cal dysfunctions, cervical muscles weakness has been suggested to be related to
pain or to fear of pain [53]. A possible explanation of patients’ sensation of weak-
ness or heaviness is the reflex inhibition of muscle due to pain that can be contrasted
only by central voluntary effort [56].
Conclusion
On the origin of the symptoms caused by whiplash, there is a wide debate espe-
cially regarding the late whiplash syndrome. Different nonorganic explanations
have been proposed as the influence of psychological factors and the possibility of
malingering. Indeed, the subjective nature of the majority of symptoms and the
possibility of a financial compensation create the basis of the so-called compensa-
tion hypothesis. This theory is supported by the evidence that the incidence of
whiplash syndrome varies between nations with different insurance systems and
that the number of claims decreases after modification in financial compensation
[57]. However, there are currently no sufficient data to accept this hypothesis [58].
The controversy between the organic and nonorganic etiology of whiplash has to
be kept in mind to understand the conflicting data reported above.
In conclusion, irrespective of scientific debate, clinicians should carefully
evaluate neurological symptoms to address patients to the correct diagnostic cen-
ter and to choose the most appropriate treatment. Nevertheless, it is mandatory to
consider the psychological aspects of this condition to achieve a correct “prise en
charge” of the patients.
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Radiological Evaluation
7
A. Bettinelli, M. Leonardi, E.P. Mangiagalli, and P. Cecconi
7.1 Introduction
The term “whiplash syndrome” was introduced by Crowe in 1928 [1], and it is nor-
mally used to describe a group of symptoms variously associated with unequal
clinical importance. In most instances, the symptomatology is subjective, therefore
the ensuring radiological evaluation may be elusive.
Generally speaking, patients complain about continuous pain to the posterior
aspect of the occiput or the neck or both, sometimes bilaterally, with an area of
reference to one or more muscles of the cervical paravertebral musculature; the
trapezius is the muscle more frequently involved and, not uncommonly, there is a
trigger zone lying outside the painful area [2]. The pain may irradiate to the axilla,
to the arm, to the superolateral portion of the chest, and to the inferior tip of the
shoulder blade. It is frequently associated with vertigo, tinnitus, diplopia, and dys-
phagia. In all such cases, the neurological exam is normal.
The pain worsens with movements of the cervical spine or with the strain
involved in maintaining a posture.
Despite a large number of rear-end collisions on the road and a high frequency
of whiplash injuries were reported, the mechanism of whiplash injuries is not
A. Bettinelli (*) • E.P. Mangiagalli

Intermedica s.r.l., “Columbus” Private Hospital,
via Buonarroti 48, Milan, Italy
e-mail: intermedicarm@libero.it
M. Leonardi
Department of Neuroradiology, “Bellaria” Hospital,
via Altura 3, Bologna, Italy
P. Cecconi
Department of Neuroradiology, IRCCS “Don Carlo Gnocchi” Foundation,
via Capecelatro 66, Milan, Italy
e-mail: pcecconi@dongnocchi.it

66 A. Bettinelli et al.
completely understood. One of the reasons is that the injury is not necessarily
accompanied by obvious tissue damages detectable by X-ray or MRI.
Based on kinematical studies on cadavers and volunteers, there are three distinct
periods that have the potential to cause injury to the neck. In the first stage, flexural
deformation of the neck is observed along with a loss of cervical lordosis; in the
second stage, the cervical spine takes an S-shaped curve as the lower vertebrae
begin to extend and gradually cause the upper vertebrae to extend; during the final
stage, the entire neck is extended due to the extension moments at both ends.
Experimental findings have examined strains across the facet joint as a mecha-
nism of whiplash injury and suggested a capsular strain threshold or a vertebral
distraction threshold for whiplash-related injury, potentially producing neck pain.
Injuries to the facet capsule region of the neck are a major source of post-crash
pain. There are several hypotheses on how whiplash-associated injury may occur
and there are several possible injury criteria to correlate to the duration of symp-
toms during reconstructions of actual crashes. On a biomechanical basis, it has
been hypothesized that the facet joint capsule is a source of neck pain and that the
pain may arise from large strains in the joint capsule that will cause pain receptors
to fire.
The aim of the chapter is to show the role of imaging in detecting and demon-
strating spine and cervical soft tissues involvement due to whiplash.
7.2 Plain Standard X-Rays
Timely and accurate diagnosis of cervical spine injury is essential. A complete

cervical spine series will diagnose almost 90 % of all cervical spine injuries and
consists of a lateral roentgenogram from C1 to the top of T1, an AP roentgeno-
gram, and an open mouth view (odontoid). In patients with large shoulders and/or
short neck, it is often difficult to visualize the C7-T1 junction on the lateral film,
and it may be necessary to apply traction to the arms to pull down the shoulders or
obtain a swimmer’s view [3]. Radiographs of the cervical spine after a whiplash
injury are generally normal, except for the possible loss of physiological cervical
lordosis [4].
The plain standard X-ray projections (anteroposterior, latero-lateral, oblique)
obtained with the patient either in standing or sitting position may show a reversal
of the physiological lordosis up to a hyperkyphotic appearance, sometimes coexist-
ing with a lateral flexion of the cervical spine due to contraction of the lateral mus-
cles of the neck. In this case, some authors [2] infer that the spasm of the neck
muscle may be very disabling (i.e., in children it often reaches the features of a
posttraumatic torticollis), especially if unilateral, and may interfere with the pos-
tural reflex of the neck ensuing a continuous and annoying vertigo which affects
ambulation. Even a sprain to the longissimus colli may be associated with an injury
of the cervical sympathetic plexus causing nausea and vertigo [2].
In the lateral projection, a widening of the vertebral interspace and perching of
the facet joints can be noted due to a lesion of their facetal joint capsule. For this
7 Radiological Evaluation 67
reason, lateral flexion and extension radiographs are useful to demonstrate the
possible presence of an abnormal motion of one or more cervical vertebra disclos-
ing injuries of the ligaments complex [5].
When an angular kyphosis is present, then an anterior or posterior subluxation
may often be demonstrated, and the upper vertebral body is posteriorly or anteriorly
displaced. Widening of the distance between the spinous processes (fanning) may
be noted due to disruption of the interspinous and posterior ligament [29]. After a
congruous period of time, discal and arthrosic modifications develop at the site of
the kyphotic angulation.
Oblique radiographs in patients with flexion distraction injuries can be useful in
the diagnosis of facet fractures. Obviously they should be obtained by angling the
radiograph beam and not rotating the patient’s head.
Pluridirectional tomography appears to be particularly advantageous in patients
with injuries involving the facets. Computerized tomography appears to add the
most additional information in patients with laminar and posterior element fractures
and C1 fractures.
In unilateral dislocation on a lateral plain roentgenogram, the cephalad vertebra
may appear translated up to 25 % of the width of the caudal vertebral body with
splaying apart of the posterior spinous processes: The rotational deformity allows
visualization of both facet joints on the lateral roentgenogram (normally superim-
posed), the so-called bow tie sign. On the AP roentgenogram, the spinous processes
may be rotated with widening of the interspinous distance.
With bilateral dislocations, both inferior articular processes of the cephalad ver-
tebra dislocate anterior to the superior processes of the caudal vertebra: This results
in approximately 50 % anterior translation of the superior vertebral body on the
inferior vertebral body. There is no rotational deformity (absent bow tie sign) on
roentgenographic evaluation, and clinically the patient’s head is held in the
midline.
It is also very important not to neglect the first part of the thoracic spine, because
it is not rare to see vertebral body fracture in T1 to T4. In fact, these vertebrae are
functionally ascribed to the cervical spine by many authors.
Finally, the lower back must not be forgotten, because it is not rare that accident
can involve this part of the body as well.
The role of dynamic lateral radiographs in an emergency setting remains contro-
versial. These views are useful in alert, cooperative patients without neurological
deficit and a normal spine series who continue to complain of neck pain. In this
setting, a positive flexion-extension study has obvious clinical implications, but a
negative roentgenogram does not rule out an acute flexion distraction injury. Patients
with acute cervical spine subluxation may have muscle spasm which masks cervical
instability for up to 2–3 weeks [5].
Static or dynamic flexion/extension lateral plain and AP roentgenogram can
show subluxation of cervical vertebrae. Subluxation of the posterior cervical facet
joints is caused by a partial disruption of the articular capsule and possibly the inter-
vening intervertebral disk which allows anterior translation of the cephalad vertebra
on the more caudal vertebra.
7.3 CT Scan
CT scan has no indication in the evaluation of patient with whiplash syndrome as

we defined it here. Although CT allows good visualization of the bony structures, it
does not yield a study of the ligamentous complex. CT with 3-D programs may
demonstrate bony lesions not otherwise appreciated. It is true, CT permits imaging
of the cervical disks and their lesions; however, an acute posttraumatic cervical disk
herniation is very seldom without neurological deficits. Hence, within the frame-
work of this chapter, CT evaluation is usually normal.
7.4 Magnetic Resonance Imaging
MRI clearly visualizes the anterior and posterior longitudinal ligaments and the
interspinous ligament; hence, it is useful in defining their eventual tear. With the
appropriate sequences, MRI permits evaluation of the soft tissues and the muscles.
The presence of edema and/or hemorrhage in such spinal structures produces altera-
tion in the magnetic signal [6].
MR imaging at 1.5 T reveals only limited evidence of specific changes to the
cervical spine and the surrounding tissues in patients with acute symptomatic whip-
lash injury compared with healthy control subjects [7], but it is the choice imaging
exam for cervical spine when radiographs show pathological findings or the clinical
examination demonstrated signs suggestive of medullar involvement. The choice
depends on the ability to show soft tissues and particularly nervous structures better
than CT.
The principal disadvantage of MRI is the inability to show the cortical bone,
making difficult the diagnosis of small fractures or the revelation of displaced bony
fragments.
In the acute phase, plain radiographic films may only disclose, in lateral neutral
position, a straightening or reversal of the physiological lordosis, or in lateral
flexion-extension projection, an increased mobility of the cervical spine. In a
selected number of patients, MRI may demonstrate the presence of paravertebral
soft tissue edema or hematoma in the muscle of the neck.
Hypothesis that loss of integrity of the membranes in the craniocervical junction
might be the cause of neck pain in patients with whiplash-associated disorders
(WADs) has been proposed [8, 9]. In recent years, with the development of more
detailed imaging techniques, morphologic changes of the ligaments and membranes
in the craniocervical junction, especially alar and transverse ligaments, have been
discussed. A meta-analysis was performed by Li et al. [10] to evaluate the relation-
ship of MRI signal changes of alar and transverse ligaments and WADs. According
to the authors, MRI signal changes of alar and transverse ligaments are not sup-
posed to be caused from whiplash injury, and MRI examination of alar and trans-
verse ligaments should not be used as the routine workflow of patients with WADs.
Schmidt et al. [11] demonstrate that high-field 3-T MRI provides better visual-
ization of the alar ligaments compared with 1.5-T MRI. The higher signal-to-noise
ratio allows detection of small signal changes. A great interindividual variety of the
MRI morphology of the alar ligaments was found in participants with no history of
neck trauma. Rupture of the alar and transverse ligaments due to whiplash injury
can lead to upper cervical spine instability and subsequent neurological deteriora-
tion. The purpose of their study was to evaluate the normal anatomical variability of
the alar ligaments in asymptomatic individuals with 3-T magnetic resonance imag-
ing and to compare the findings with standard 1.5-T examinations. Magnetic reso-
nance imaging findings were analyzed by classifying the alar ligaments with regard
to the features detectability, signal intensity compared with muscle tissue, homoge-
neity, shape, spatial orientation, and symmetry. Delineation of the alar ligaments
was significantly better on 3-T images, which were subjectively preferred for evalu-
ation. The alar ligaments showed great variability. In the majority of participants,
the alar ligaments were hypointense to muscle tissue, inhomogeneous, and different
in shape and orientation.
Lummel et al. [12] showed an high variability of rotational mobility at the cra-
niocervical junction and an attenuation of width of the subarachnoid space during
head rotation also in an asymptomatic population. Their results indicate that the
assessment of these parameters is of limited diagnostic value in patients with
whiplash-associated disorders.
Cervical muscles involvement can be specifically investigated by mean of MRI.
According to Elliot et al.’s [13] current evidence from structural MRI-based studies
demonstrates the widespread presence of fatty infiltrates in neck muscles of patients
with chronic whiplash. Such findings have not shown to feature in patients with
chronic insidious-onset neck pain, suggesting traumatic factors play a role in their
development. Recent studies have revealed that muscle fatty infiltrates manifest
soon after whiplash but only in those with higher pain and disability and symptoms
of posttraumatic stress disorder. The possibility that such muscle changes are asso-
ciated with a more severe injury including poor functional recovery remains the
focus of their research efforts. Authors hypothesized that cervical muscle hypotro-
phy would be evident after a 6-month follow-up and that cervical muscle hypotro-
phy would correlate with symptom persistence probably related to pain or inactivity.
They performed in 90 symptomatic patients (48 females) MRI cross-sectional mus-
cle area (CSA) measurements, bilaterally, of the cervical extensor and sternocleido-
mastoid muscles using transverse STIR (short tau inversion recovery) sequences at
the C2 (deep and total dorsal cervical extensor muscles), C4 (sternocleidomastoid
muscles), and C5 (deep and total dorsal cervical extensor muscles) levels. They
found that women consistently had smaller CSAs than men. They found no signifi-
cant changes of CSAs over time at any of the three levels. There were no consistent
significant correlations of CSA values with the clinical scores at all time points,
except with the body mass index. In conclusion, authors did not support a major role
of cervical muscle volume in the genesis of symptoms after whiplash injury.
Long-term follow-up studies focusing on the posterior extensor muscles in
patients suffering from whiplash injury are scarce. The purpose of Elliot et al. study
[14] was to elucidate the changes in the posterior extensor muscles 10 years after
whiplash injury. They performed MRI using a 1.5-T superconductive imager in 23
patients who had suffered from whiplash injury in 1994–1996 (13 males, 10 females,
mean age 51.8 years, mean follow-up 11.5 years). In addition, 60 healthy volunteers
who had undergone MRI in the same period were included as controls (36 males, 24
females, mean age 47.8 years, mean follow-up 11.1 years). All participants under-
went follow-up MRI. The cross-sectional areas of the deep posterior muscles (CSA)
including the multifidus, semispinalis cervicis, semispinalis capitis, and splenius
capitis were digitally measured at C3–C4, C4–C5, and C5–C6 using NIH image.
The long-term changes in the CSA were compared between the two groups. In addi-
tion, correlations between the CSA and cervical spine-related symptoms were eval-
uated. The mean total CSA per patient (the sum of the area from C3–C4 to C5–C6)
was 4811.6 ± 878.4 mm2 in the whiplash patients and 4494.9 ± 1032.7 mm2 in the
controls at the initial investigation (p = 0.20) and 5173.4 ± 946.1 mm2 and
4713.0 ± 1065.3 mm2 at the follow-up (p = 0.07). The mean change in CSA over
time was 361.8 ± 804.9 mm2 in the whiplash patients and 218.1 ± 520.7 mm2 in the
controls (p = 0.34). Ten whiplash patients (43.5 %) had neck pain and 11 (47.8 %)
had shoulder stiffness. However, there was no difference in the change in CSA over
time between the symptomatic and asymptomatic patients. In conclusion, authors
showed no significant difference in the change in CSA between whiplash patients
and healthy volunteers after a 10-year follow-up period. In both groups, the cross-
sectional area slightly increased at follow-up. In addition, there was no association
between the change in CSA and clinical symptoms such as neck and shoulder pain.
These results suggest that whiplash injury is not associated with symptomatic atro-
phy of the posterior cervical muscles over the long term [15–18].
Modic changes (MC) are a common phenomenon on magnetic resonance imag-
ing (MRI) in spinal degenerative diseases and strongly linked with low back pain.
They are due to signal intensity changes of vertebral endplates and subchondral
bone. In 1988, Modic et al. [19] summarized these changes and classified them into
three types, and then modic changes (MC), as a medical term, were used in the stud-
ies on spinal degenerative diseases.
There are few studies on MC of the cervical spine in patients suffering from
whiplash. Matsumoto et al. [20] investigated relationships between modic changes
and clinical symptoms or potentially related factors. They showed that while modic
changes became more common in whiplash patients in the 10-year period after the
accident, they occurred with a similar frequency in control subjects. We did not find
any association between modic changes and the nature of the car accident in which
the whiplash occurred. Modic changes found in whiplash patients may be a result of
the physiological ageing process rather than pathological findings relating to the
whiplash injury.
MRI can be used also to investigate extra-vertebral cervical involvement [21].
Elliot et al. through a [22] cross-sectional investigation has identified reductions in
the size and shape of the oropharynx in subjects with chronic whiplash-related dis-
ability when compared to healthy controls. Repeated T1-weighted magnetic reso-
nance imaging was used to measure and compare cross-sectional area (CSA) in
square millimeters and shape ratio (SR) of the oropharynx in subjects with acute
whiplash injury. MRI was performed at 4 weeks, 3 months, and 6 months
post-injury. Subjects were classified at 6 months by their Neck Disability Index

scores into the following categories: recovered (less than 8 %), mild disability (10–
28 %), and moderate/severe disability (greater than 30 %). The effects of time and
group and the interaction effect of group by time on oropharynx [23] morphometry
(CSA, SR) were investigated using repeated-measure, linear, mixed-model analy-
sis. Based on previous research findings, age, gender, and body mass index were
entered into the analyses as covariates. Where significant main or interaction effects
were detected, pairwise comparisons were performed to investigate specific differ-
ences in the dependent variable between groups and within groups over time.
Authors found a significant interaction effect for group by time for both the CSA
and SR values. Age significantly influenced SR, and body mass index significantly
influenced CSA – there was no difference in CSA or SR across all groups at 4 weeks
post-injury. However, at 6 months, CSA was significantly different between the
recovered group and the moderate/severe group. The recovered group demonstrated
a significant increase in CSA over time, whereas the moderate/severe group signifi-
cantly decreased. At 6 months, the moderate/severe group had a reduced SR com-
pared to the mild group. No differences in CSA or SR of the oropharynx were found
between the mild and recovered groups throughout the study. In conclusion, authors
showed temporal reductions in CSA of the oropharynx occur following whiplash,
reductions that persist to a greater extent in those with moderate/severe symptoms
at 6 months post-injury.
7.5 Echography and Duplex Sonography
Echography of the cervical soft tissue has to be considered as a second-level inves-

tigation. It can be used to depict the size of the cervical multifidus muscle in asymp-
tomatic and symptomatic subjects [24]. The cross-sectional area (CSA) and the
transverse versus the anterior-posterior dimensions (shape ratio) are measured at the
C4 level. The size of the multifidus muscle may be significantly reduced in symp-
tomatic subjects, which indicates loss of clarity of the fascial layer between the
semispinalis cervicis muscle and the cervical multifidus muscle. In this way, echo-
graphic findings, in long-lasting symptomatic patients, may be a diagnostic sign of
muscle atrophy [25].
Whiplash can induce lesion of deep oro-cervical soft tissues like retropharyngeal
hematoma, resulting in airway obstruction and mortality due to bleeding amongst
deep cervical fascias. Echography is the examination of choice when this situation
is suspected [26].
Transcranial Doppler (TCD) sonography may be used for the assessment of ver-
tebrobasilar circulation in patients with a whiplash injury of the cervical spine. Seric
et al. [27] examined a group of WAD patients by TCD within a month and then 6
months following the accident. The obtained values were compared to normal blood
flow velocities and correlated with the severity of clinical picture. During the first
month after the injury, statistically significant disturbances in the vertebrobasilar
circulation were recorded, such as the increase in mean blood flow velocities in
Table 7.1 Radiological strategy

Early trauma
Plain standard X-rays
Normal Bone lesion? Posture abnormalities Facets abnormalities
Stop CT scan Dynamic radiograms/echography MRI
Late trauma
Plain standard X-rays
Normal Arthrosis Arthrosis Posture abnormalities
Without neurological With neurological symptoms Without arthrosis
symptoms
Stop Stop MRI Dynamic radiogram
and/or echography
AVL (68 %), AVR (62 %), and BA (51 %) (mostly as spasm). Six months later,
normal findings were obtained in about 50 % of the vessels, whereas in the rest of
the patients, vasospasm persisted in one, two, or all examined blood vessels.
TCD of the vertebrobasilar circulation is a very useful method in the diagnostics
and follow-up of patients with a whiplash injury. Vertebral artery flow evaluation
can be considered an effective supplementary method in a precise workup espe-
cially in polytrauma patient as well as in patients presenting with delayed onset of
symptoms; in fact the V3 segment of the vertebral artery, especially where it courses
through its groove behind the superior facet of the atlas, is particularly vulnerable to
injury. Flow velocity is measured at the V3 segment from a point just below and
roughly 2–3 cm dorsal to the mastoid process [28].
Conclusions
At a later date the neutral lateral view may reveal the evolution of a reversed
lordosis in an angular kyphosis with the presence of a narrowed intervertebral
space and an unco-arthrosis.
However, it can be very difficult to correlate patient’s claim with X-ray find-
ings, especially if the radiological evaluation is “normal or almost normal.”
Posttraumatic disturbances may be present and, in some cases, disabling even
with a normal radiological examination. Radiological strategy is presented in
Table 7.1. Planning CT scan or MRI or echography is partially based on X-ray
plain findings but mostly on clinical symptoms and signs.
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Part II
Pathophysiology
The Vestibulo-vertebral
Functional Unit 8
D.C. Alpini, G. Brugnoni, A. Cesarani, and P.M. Bavera
8.1 Introduction
The importance of the head as reference in dynamic control of balance is supported

by evidence that the head itself supports three type of sensors: the vestibular system,
which is sensitive both to gravity forces and head itself accelerations; vision, which
is able to stabilise the head and the body with respect to the external space; and the
neck muscle’s proprioceptive input which conveys the position of the head with
respect to the trunk providing an ‘error signal’ to central vestibular system in order
to optimise vestibulo-spinal control.
The head stabilised in space serves as a reference frame for the postural organisa-
tion of the rest the body. In fact, while vertical alignment and centre of pressure
displacement control during quiet standing are strictly important in postural control,
head stability is important for balance in dynamic conditions like walking [1]. Static
and dynamic head stabilisation is obtained through proper tonic and phasic contrac-
tion of the cervical muscles. Due to spine biomechanics, also dorsal and paraverte-
bral muscles contribute to head stabilisation in space.
D.C. Alpini (*) • P.M. Bavera

ENT-Otoneurology Service, IRCCS “Don Carlo Gnocchi” Foundation,
Milan, Italy
G. Brugnoni
Italian Academy of Manual Medicine,
Italian Institute for Auxology, Milan, Italy
e-mail: guido.brugnoni@libero.it
A. Cesarani
Audiology Unit, IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico,
Milan, Italy

78 D.C. Alpini et al.
For these reasons, it is possible to define the co-operation between vestibular

cues and vertebral muscles activity as a functional unit, that is to say, the vestibulo-
vertebral unit.
Because head stabilisation occurs during different tasks and conditions, some
investigators speculate that motor system utilises a top-down control schema. The
top-down schema corrects head displacements preventing upward transmission of
movements from the trunk so that head remains stable in the space providing an
inertial guidance system [2]. Stabilisation of head is thought to improve the inter-
pretation of vestibular input for balance. In fact, head stabilisation reduces the iner-
tial acceleration on otolithic membrane and semicircular canals, improving the
estimation of gravitational acceleration and providing a stable gravitational refer-
ence. Head stabilisation also decreases the retinal slip of the image of the world on
the retina and, in the specific, decreasing of retinal slip allows a more accurate
visual control of the environment. Head control is not directly influenced by input
from sensorial systems; rather, complex high order of sensory mechanisms combine
inputs, forming frames of reference; so each sensory cue has a value of reference
against which the changes of signal is interpreted. Finally, frames of reference of
each cue are used to create body schema that is defined as ‘a combined standard
against which all subsequent changes of posture are measured’.
The internal representation of body schema allows CNS to represent body geom-
etry, body kinetics and the attitude of the body with respect to gravity.
The importance of different body parts in the definitions of body schema relies
on the specific characteristic of each segment itself. For example, the feet inform the
position and attitude of support surface and the forces that are exerted by the sup-
port surface on the body; the importance of the trunk in the representation of body
schema is justified by the fact that the trunk is the segment with bigger mass; a pri-
mary role of head in body schema is justified by the fact that visual and labyrinthine
systems are located in the head and inform on the position of line of gravity and the
horizontal; moreover, inputs from neck proprioceptors control the relationship
between trunk and head.
This process leads to a better evaluation of the movement of the body segments
with respect to the segment of reference and the position of the subjects with respect
external world.
Vestibular function is dependent also by blood supply and venous drainage.
Vascular inner ear system is regulated by sympathetic and parasympathetic cervical
system. In this way, into the so-called vestibulo-vertebral functional unit, vascular
and autonomic cervico-cephalic systems have to be taken in account.
8.2 Head Stabilisation Control
8.2.1 Vestibular Reflexes
During each movement of the head and/or body, it is necessary that the image of the
perceived surrounding has to remain on the same place on the retina [3]. Thus, the
8 The Vestibulo-vertebral Functional Unit 79
image of the perceived part of the environment must be changed in a very quick
way. During head movement, the eye has to make movements relative to the skull
in such a way as to guarantee immobilisation of the image projection on the retina.
If there is a ‘retinal sip’, the vision is blurred, and the surrounding is perceived as
moving around. As a result, during head movement, that required eye movement
has to be ‘compensatory’, in order to cancel the effect of the head movement. Such
an eye movement is executed in a reflective manner, without conscious interven-
tion, and it is called vestibulo-ocular reflex (VOR).
The achievement of correct erect standing position, both in static and in dynamic
conditions, requires continuous adaptation of counterreaction of antigravity mus-
cles to the gravity force, in order to stabilise head position and to maintain erect
position itself. Maintaining of upright position of the body is acquired via a con-
tinual to and fro movement of the centre of gravity (CoG) around the point of mass
equilibrium. This movement is called ‘postural sway’. It is achieved in a reflective
manner by the mean of the so-called vestibulo-spinal reflexes (VSR). The control of
correct head position is possible through the activation of the neck muscles by the
mean of a part of the VSR (the so-called vestibulo-collic reflex, VCR) and the cervi-
cal reflexes.
8.2.2 Cervical Proprioception
The receptors of the cervical region play a separate and particular role and consti-
tute what can be considered as a ‘secondary labyrinth’ [3]. In a clinical context,
attention has been devoted to the neck with respect to a possible origin of vertigo,
the so-called cervical vertigo. Furthermore, its role in the posture of the head and
the body seems undeniable. The cervical region with its structures intervenes in the
elaboration of balance reflexes. Neck-body reflexes as well as cervical influences
upon eye position have been described. It is the task of neck proprioceptors to
inform the centres about movement or change of position of the head, so far as this
concerns a differential movement between head and trunk. This is the fundamental
difference from the vestibular system which is sensitive to head movements relative
to space. Both sensory systems provide specific and proper information, thus com-
plementing one another.
Peripheral proprioceptors of the muscles and the joints have a feedback control
on the vestibular nuclei through spino-vestibular pathways. Neuromuscular spin-
dles and Golgi receptors are dynamometers, and they are particularly sensitive to
variations in muscle length and tension. Joint receptors, Ruffini corpuscles and
Golgi bodies give information regarding the position of a joint and its movement.
The portion of the neck including the first three vertebrae is particularly involved
during the major part of everyday head movements. The paravertebral muscles of
this region are very rich in proprioceptors. They are especially concentrated in the
splenius capitis, the rectus capitis major, the longissimus capitis and the semispi-
nalis capitis. These muscles compose the deep plane of the nuchal muscles. The
splenius is just more superficial. They act in the extension homolateral bending and
rotation of the head. During head movements they discharge to the vestibular
nuclei.
Direct projection from the first three cervical roots to the inferior vestibular
nucleus has been described as well as the convergence of cervical and labyrinth
inputs on vestibular nuclei has been showed. Convergence regards especially inputs
from horizontal semicircular canal: the electrical stimulation of the vestibular nerve
induces action potentials in the contralateral abducens nerve. This response is
increased when also neck roots are contemporary stimulated. Thus, facilitatory con-
vergences of proprioceptive inputs from C2 to C3 receptors on the medial vestibular
nucleus of the opposite side and an inhibition on the ipsilateral muscles have been
demonstrated. The latency between electrical stimulation of the dorsal cervical
roots and vestibular nucleus response is only 2 ms; thus, direct projections from
neck to vestibular nuclei have been hypothesised. Proprioceptive nuchal afferences
on the Schwalbe nucleus have been demonstrated as well as it has been shown that
neurons in the dorso-caudal portion of the Deiters nucleus receive tonic cervical
inputs, while the neurons in the rostro-ventralis portion receive especially otolithic
inputs. Roller nucleus and the accessory group Y receive ipsilateral projections
from the cervical muscles, and cerebellar projections on the nodulus and the floc-
culus have been demonstrated as well as projections on the cerebellar anterior lobus
have been described.
Proprioceptive convergences in 80 % of the neurons in the suprasylvian parietal
cortical vestibular area have been demonstrated and sensitive inputs run through IA
and IIA fibres that raise along spinal cord and through the spino-reticular and
spino-cerebellar fasciculus that seem to send direct projections to the vestibular
nuclei.
From cervical proprioceptors arise the cervico-spinal reflexes (CSR): bending
the neck and turning the head relative to the body evokes reflexes in the limb mus-
cles either in decerebrate cats or in human beings.
These reflexes interact with the vestibulo-collic reflex (VCR) which is a part of
the vestibulo-spinal reflexes (VSR).
Vestibulo-collic reflex moves the head and interferes with the VOR for stabilis-
ing the visual field. The VCR rotates the head in the plane of the canal. Natural canal
stimulation results in contraction of neck muscles to counter the applied angular
acceleration and thus results in stabilisation of the head. VCR augments the VOR
for image stabilisation during head movement. Cervico-ocular reflex and cervico-
collic reflex act to generate compensatory shifts of gaze which opposed those pro-
duced by rotation of the head. While the gain of COR is too small to make a
significant contribution to gaze stability, the CCR is capable of generating large
changes in neck muscles activity, which influences gaze and head position. In con-
trolling gaze, the VCR and CCR damp oscillations of the head and produce counter-
rotations that partially compensate for the rotation of the body, while the VOR
compensates for residual rotation of the head with respect to space. In animals with
vestibular lesions, COR and CCR increase to compensate partially. Head stabilisa-
tion contributes to gaze stabilisation [4].
8.3 Interaction Between Ocular Stabilisation Reflexes

in Patients with Whiplash Injury
8.3.1 Autonomic Cervico-cephalic System
8.3.1.1 Sympathetic Supply to the Head and Neck

The preganglionic fibres, which supply the head and neck, arise from the spinal seg-
ments T1 to T2. They enter the sympathetic trunk and travel upward to synapse in
one of the three ganglia in the neck:
1. The superior cervical ganglion (located anterior to vertebrae C1, C2)
2. The middle cervical ganglion (small, often absent, lying anterior to C6)
3. The inferior cervical ganglion which is usually fused with the first thoracic gan-
glion to form the cervicothoracic (or stellate) ganglion (located anterior to C7
and the neck of the first rib)
Each of these ganglia gives rise to:
1. Cardiac branches.
2. Branches to blood vessels, sweat glands, and hair follicles in the neck and head.
The superior ganglion sends branches to spinal nerves C1–C4, the middle gan-
glion to spinal nerves C5–C6 and the cervicothoracic ganglion to spinal nerves
C7, 8–T1.
3. Vascular branches which pass to the vertebral, common, internal and external
carotid arteries. Some of these branches ‘hitchhike’ along the arteries and their
branches to reach their targets in the head and neck. The superior ganglion sends
branches along the internal and external carotid arteries to reach structures in the
orbit, face, nasal and oral cavities and pharynx. The middle ganglion sends branches
along the inferior thyroid artery to reach the larynx, trachea and upper oesophagus.
The inferior ganglion sends branches to the subclavian and vertebral arteries.
8.3.1.2 Parasympathetic Supply to the Head and Neck

(See Also Chap. 10)
There are four ganglia in the head: ciliary, pterygopalataline, otic and
submandibular.
The parasympathetic fibres of the oculomotor nerve enter the orbit with the infe-
rior division of the nerve and synapse in the ciliary ganglion, which is located just
lateral to the optic nerve. The postganglionic fibres with the short ciliary nerves enter
the eye to supply the sphincter pupillae (that constricts the pupil) and ciliary muscles.
Parasympathetic fibres also travel along the superior branch of the oculomotor nerve
to supply the smooth muscle component of levator palpebrae superioris.
The parasympathetic fibres of the facial nerve supply the lacrimal gland, the
mucous glands of the nose and palate and the submandibular and sublingual salivary
glands. The fibres which supply the lacrimal, nasal and palatine glands leave the
facial nerve (at its genu inside the petrous bone as the greater petrosal nerve), pass
through the pterygoid canal (at the root of the pterygoid process as the nerve of the
pterygoid canal) and terminate in the pterygopalatine ganglion (located in the pter-
ygopalatine fossa). The postganglionic fibres travel in the branches of the ganglion
or the maxillary nerve to reach the nasal and palatine glands. Other preganglionic
fibres leave the facial nerve in its chorda tympani branch. This nerve passes over the
internal surface of the tympanic membrane before emerging from the skull through
a small fissure, the petrotympanic fissure, in the temporal bone. It joints the lingual
nerve (a branch of the mandibular nerve) to travel to, and synapse in, the subman-
dibular ganglion, which is suspended from the lingual nerve. The postganglionic
fibres either pass into the submandibular gland or rejoin the lingual nerve to reach
the sublingual gland.
The parasympathetic fibres of the glossopharyngeal nerve supply the parotid
gland. The preganglionic fibres travel with the tympanic branch into the tympanic
plexus in the middle ear. The fibres emerging from this plexus as the lesser petrosal
nerve, which synapses in the otic ganglion (located medial to the mandibular nerve,
just below the foramen ovale). The postganglionic fibres then hitchhike the auricu-
lotemporal nerve (a branch of the mandibular nerve) to reach the parotid gland.
8.3.2 The Cervico-oto-ocular Interaction
Interspecies and human neuroanatomy provides the most important advances on the
influence of some tracts and cortical areas on others and how they may be felt as
secondary sensorineural otic symptoms.
The protagonism of constant deep pain, trigemino-vascular auditive control,
somatosensorial-auditory multimodal integration, cortical and subcortical sound broad-
band interpretation, corticofugal modulation and limbic behavioural interferences as
CNS phenomena has been demonstrated in referred otic symptom pathophysiology.
In 2005 and 2007 Franz et al. [5, 6] widely investigated the neurophysiological
connections between inner ear and intrinsic ocular function, connections mediated
via trigeminal nerve and cervical sympathetic system.
They focused their attention to Ménière’s disease. Ménière’s disease not only
includes the symptom complex consisting of attacks of vertigo, low-frequency
hearing loss and tinnitus but comprises symptoms related to the Eustachian tube, the
upper cervical spine, the temporomandibular joints and the autonomic nervous sys-
tem. Particularly these AA observed some patients presenting normal hearing lev-
els, a mild Eustachian tube dysfunction, mydriasis on the side of the affected ear and
a functional disorder of the upper cervical spine. These patients were given a diag-
nosis of cervicogenic oto-ocular (COO) syndrome.
Authors described hypothetical reflex (Fig. 8.1) pathway that links joint injury and
the autonomic nervous system, where Eustachian tube function is under their influ-
ence and is the critical link. In this hypothetical reflex pathway, irritation of facet
joints can first lead to an activated anterior cervical sympathetic system via an inde-
pendent pathway in the mediolateral cell column; it can simultaneously lead to an
axon reflex involving nociceptive neurons, resulting in neurogenic inflammation and
the prospect of a Eustachian tube dysfunction. The Eustachian tube dysfunction is
responsible for a disturbed middle ear-inner ear pressure relationship. This reflex
Hypothetical neuronal pathway IN C1-C2

facet joint disorders
Trigeminal
ganglion
ET
IRIS
C1/2
C2
Facet
SCG joint
T2
Fig. 8.1 The pathway that links first cervical joints and the autonomic nervous system, influenc-
ing Eustachian tube function. In this hypothetical reflex pathway, irritation of facet joints can first
lead to an activated anterior cervical sympathetic system via an independent pathway in the medio-
lateral cell column. The trigeminal nerve, whose afferents come from temporomandibular joint
(TMJ), contributes to modulate both middle (Eustachian tube) and inner ear function (blood flow
regulation and thus endolymph production) and intrinsic oculomotricity (original figure by prof.
Burkhard Franz, Melbourne, Australia, with permission of the Author)
pathway is supported by recent animal experiments [7]. These experiments highlight

also the role of trigeminal nerve. Temporomandibular joint (TMJ) trigeminal afferents
contribute to modulate both middle (Eustachian tube) and inner ear function (blood
flow regulation and thus endolymph production) and intrinsic oculomotricity.
An integral model concerning neurological, anatomical and physiological per-
spectives offers a wider angle for the multiple auditory innervation patterns involv-
ing the trigeminal nerve. Vass et al. [8–10] found that trigeminal vascular system
innervation in guinea pigs controls cochlear and vestibular labyrinth function. This
plays an important role in regulating and balancing cochlear vascular tone and ves-
tibular labyrinth channel and may be responsible for the symptomatic complexity of
some cochlear diseases related to inner ear blood flow. Trigeminal ophthalmic fibre
projection to the cochlea through the basilar and anterior inferior cerebellar arteries
may play an important role in vascular tone in quick and vasodilatatory responses
to intense noise. Inner ear diseases that produce otic symptoms such as sudden hear-
ing loss, vertigo and tinnitus can originate from reduced cochlear blood flow due to
the presence of abnormal activity in the trigeminal ganglion.
Link between TMJ, trigeminal nerve and middle ear has an embryological expla-
nation. TMJ development and other neighbouring structures in humans (such as
pharynx, Eustachian tube and tympanic cavity) are complex. The mandible is formed
from the ventral part of Meckel’s cartilage, which is the first branchial arch. The
ossicles (malleus, incus and partially the stapes) are formed from the dorsal part of
Meckel’s cartilage and Reichert’s cartilage (second branchial arch). The malleus has
a double origin in these ossicles; the anterior process originates from mesenchymal
cells (os goniale), through intramembranous ossification, and the rest form from
Meckel’s cartilage, through endochondral ossification. The malleus is related to the
TMJ (condylar and temporal blastemas) by fibrous connections (lateral pterygoid
muscle) passing through the petrotympanic fissure, which Rees named the discomal-
leolar ligament. These lateral pterygoid muscular fibrous connections then form the
interarticular disc in Meckel’s cartilage by mechanical stimulation of this muscle.
Neurological, vascular and ligamental communication between the TMJ and the
middle ear is preserved during TMJ development and continues during adult life
because of continuity of Meckel’s cartilage through the petrotympanic fissure (caus-
ing an incomplete closing in adults). This fissure holds the chorda tympani nerve in
its middle ear egress to the TMJ, amongst other ear-TMJ vestige structures. The
medial pterygoid muscle and the tensor tympani muscle develop from the temporal
blastema. These structures (along with the tensor veli palatini) are innervated by the
trigeminal mandibular branch (V3), in turn innervating the masticatory muscles
coming from the first branchial arch mesoderm.
The ossicular chain and middle ear muscles primarily belong to the chewing
system (i.e. embryologically) but finally serve the auditory system.
8.4 From the Neck to the Inner Ear (Through Vertebro-basilar

System)
The vertebral artery is a major artery in the neck. It branches from the subclavian
artery, where it arises from the postero-superior portion of the subclavian artery. It
ascends through the foramina of the transverse processes of the sixth cervical verte-
brae. Then, it winds behind the superior articular process of the atlas. It enters the
cranium through the foramen magnum where it unites with the opposite vertebral
artery to form the basilar artery (at the lower border of the pons).
The vertebral artery can be divided into four divisions:
1. V1 – it runs postero-cranial between the longus colli and the m. scalenus ante-
rior; it is also called ‘pre-foraminal division’.
2. V2 – it runs cranial through the foramina in the cervical transverse processes of
the cervical vertebrae C2; it is also called foraminal division.
3. V3 – it is the part that rises from C2, from the latter foramen on the medial side
of the rectus capitis lateralis, curving behind the superior articular process of the
atlas. Then, it lies in the groove on the upper surface of the posterior arch of the
atlas and enters the vertebral canal by passing beneath the posterior atlanto-
occipital membrane.
4. V4 – that pierces the dura mater and inclines medial to the front of the medulla
oblongata.
At the junction between the medulla oblongata and the pons, two vertebral arter-
ies joint into the basilar artery, forming the so-called the vertebro-basilar system,
which supplies blood to the posterior part of circle of Willis and anastomoses with
blood supplied to the anterior part of the circle of Willis from the internal carotid
arteries.
The basilar artery ascends in the central gutter (sulcus basilaris) inferior to the
pons and divides into the posterior cerebral arteries and the superior cerebellar
artery just inferior to the pituitary stalk. From the basilar artery arises the anterior
inferior cerebellar artery (supplying the superior and inferior aspects of the cerebel-
lum), as well as smaller branches for the supply of the pons (the pontine branches).
In under 15 % of people, the basilar artery gives rise to the labyrinthine artery while,
generally, the labyrinthine artery (auditory artery, internal auditory artery), a long
slender branch of the anterior inferior cerebellar artery (85–100 % cases) or basilar
artery (<15 % cases), arises from near the middle of the artery; it accompanies the
vestibulocochlear nerve through the internal acoustic meatus and is distributed to
the internal ear.
CNS interaction between the somatosensory system and multilevel vestibular
tracts cranial and cervical muscular dysfunction producing hypertonicity and mus-
cular spasm can irritate nerves and blood vessels by muscular trapping.
The vascular relationship between the TMJ and the middle ear may explain otic
symptoms in the presence of a vascular reflex from TMJ disorders. The most medial
anterior tympanic artery posterior group branches (behind the TMJ) irrigate the
tympanic cavity and the outflow of the inner ear, which is completely drained by the
vein of the cochlear aqueduct.
8.5 From the Inner Ear to the Spine (Through Venous

Drainage)
The veins of the vestibule and semicircular canals accompany the arteries and,
receiving those of the cochlea at the base of the modiolus, unite to form the internal
auditory veins (or veins of labyrinth) which end in the posterior part of the superior
petrosal sinus or in the transverse sinus [11].
The common modiolar vein enters the bony channel immediately adjacent to the
aqueduct to become the vein of the cochlear aqueduct which in turn drains via the
inferior petrous sinus into the internal jugular veins (IJVs). Injury or occlusion of
this vessel would be particularly significant since it is widely believed to provide
virtually the entire venous drainage of the cochlea [12].
The cochlear aqueduct and the internal auditory canal communicate with the
subarachnoidal space; in the guinea pig model, an occlusion of the veins of the
cochlear aqueduct results in an increase of perilymphatic endolymphatic pressure, a
decrease of cochlear blood flow and endolymphatic potential. Furthermore, since
many of the venous vessels in the scala tympani have little or no bony covering and
are essentially exposed to the perilymphatic space, the venous system is a route of
entry for the cells participating in the inner ear inflammatory process.
Another interesting point is that the blood leaves the brain by using the back
propulsion of the residual arterial pressure (vis a tergo), complemented by antero-
grade respiratory mechanisms (vis a fronte). The latter consist of the thoracic pump
increased venous outflow during inspiration: the increase of negative thoracic pres-
sure improves the aspiration of blood toward the right atrium. In addition to vis a
tergo and vis a fronte, postural mechanisms play a fundamental role in ensuring a
correct cerebral venous return.
The pattern of cerebral venous drainage changes, even under physiological con-
ditions, depending on the body position. In the prone or supine position, the outflow
through the IJVs is favoured, whereas passing to the upright position transfers most
of the encephalic drainage to the vertebral veins.
Corrosion cast study highlights the complexity of the venous network in the
craniocervical junction.
Schematically, two descending cerebral venous outflow tracks can be distin-
guished: the internal jugular veins anteriorly and the vertebral venous system poste-
riorly. The latter is composed of the external and internal vertebral venous plexuses,
which are anastomosed by way of the intervertebral and basivertebral veins.
In the cervical region, the vertebral venous system is mainly represented by the
anterior internal vertebral venous plexus, the vertebral artery venous plexus and the
deep cervical veins.
As far as this posterior outflow track is concerned, the anterior, posterior and
lateral condylar veins and the anterior condylar confluent (ACC) represent the most
important connections between the intracranial cerebral venous circulation and the
vertebral venous systems.
The posterior and lateral condylar veins allow for connections with the external
vertebral venous system, whereas the anterior condylar veins are predominantly
related to the internal vertebral venous plexus. It is noteworthy that even though the
diameters of the anterior and lateral condylar veins were important, they were con-
nected to the internal jugular vein by only a small anastomosis between the jugular
bulb or internal jugular vein and the ACC.
Venous flow from the jugular bulb through the anterior condylar vein and into
the anterior internal vertebral venous plexus occurs efficaciously by way of the
ACC regardless of how indirect this pathway might seem.
The ACC appeared as an anatomic constant whose major tributaries, size-wise,
were the anterior and lateral condylar veins, inferior petrosal sinus and internal
jugular vein. The ACC was also connected to the carotid artery venous plexus by the
inferior petro-occipital vein and to the prevertebral venous plexus. The numerous
anastomoses of the ACC make it a crossroad between the cavernous sinus, dural
venous sinuses of the posterior fossa and posterior cervical outflow tracks. ACC is
a ‘common canal’ of the inferior petrosal sinus and the anterior condylar vein of the
junction of the inferior petrosal sinus and internal jugular vein sinus posteriorly.
From a physiological point of view, one should also consider that the same pos-
tural influences affecting cerebral venous drainage might redirect the circulation of
the internal and external vertebral venous systems. For instance, the cranial
(as opposed to caudal) connections of the anterior internal vertebral venous plexus
with the anterior condylar vein could offer a cranial escape route for thoracic and
abdominal venous return when thoracic pressure and abdominal pressure are
increased concomitantly. One could even consider venous blood from the anterior
internal vertebral venous plexus draining into the superior ophthalmic vein and cav-
ernous sinus through the basilar plexus and inferior petrosal sinuses and thus termi-
nally into the pterygoid plexus and facial veins.
In conclusion, cervico-cephalic drainage system is very complex: cerebral, neuro-
cranial and cervical venous blood might take different common, but variable, outflow
tracks depending on posture, pressure and anatomic variations. Anterior, lateral and
posterior condylar veins and occipital and mastoid emissary veins provide connec-
tions between the posterior fossa dural sinuses and internal jugular vein system with
the cervical vertebral venous system. These emissary veins allow for encephalic
blood to drain into the cervical internal and external vertebral venous plexuses, which
represent the major outflow tract for encephalic drainage in the upright position.
The ACC, a venous entity ignored since Trolard described it in 1868, represents
a major venous crossroad of the base of the skull.
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Pathophysiology
of Whiplash-Associated Disorders: 9
Theories and Controversies
M. Magnusson, M. Karlberg, C. Mariconda, A. Bucalossi,

and G. Dalmazzo
9.1 Introduction
The term “whiplash” already suggests difficulties in assessing this problem. Patients
suffering from “whiplash” or “whiplash-associated disorders” (WAD) are defined
as having been exposed to similar types of trauma or sometimes even similar mode
of impact, rather than as having a certain type of lesion or set of symptoms [1, 2].
The origin of the term “whiplash” is attributed to H. Crowe [3, 4], who suggested a
trauma to the cervico-cranial junction based on the mechanism of acceleration and
deceleration of the head impact.
The Quebec task force (QTF) [5, 6] on whiplash-associated disorders (WAD)
defined whiplash as “bony or softy tissue injuries” resulting “from rear-end or side
impact, predominantly in motor vehicle accidents, and from other mishaps as a
result of an acceleration-deceleration mechanism of energy transfer to the neck.”
Whiplash is associated with a wide variety of clinical manifestations including neck
pain, neck stiffness, arm pain and paresthesias, problem with memory and concen-
tration, and psychological distress [7, 8].
Below, some different theories of the organic causes of the complaints will be
discussed, but it should be pointed out that it would not come as a complete surprise
to us if in the future it becomes apparent that several mechanisms contribute to the
complaints of the heterogeneous group of patients suffering from WAD [9].
M. Magnusson • M. Karlberg
Department of Otorhinolaryngology, Lund University Hospital,
Lund University, Lund, Sweden
e-mail: mans.magnusson@med.lu.se
C. Mariconda (*) • A. Bucalossi • G. Dalmazzo
Gradenigo Hospital, Turin, Italy
e-mail: carlo.mariconda@gradenigo.it

90 M. Magnusson et al.
9.2 Pathophysiologic Mechanisms
There are several different theories to explain the traumatic mechanisms of whip-
lash injuries, as one has to assume that in such lesions there may be concomitant
mild brain injury [10, 11]. The possible pathogeneses may include lesions to the soft
tissue of the neck, cervical roots, peripheral and central nervous neuronal tissues,
and the inner ear.
9.2.1 Lesions to Soft Tissues and Peripheral Nerves
On the one hand, it has been suggested that WAD should be distinguished from
sprained necks, traumatic disk protrusions, and damage to cord and nerve roots. On
the other hand, it is clear that, to associate the symptoms with the trauma, the patient
should present with neck pain in close connection with the trauma [12]. If the find-
ing that the pain from the neck emanates from the soft tissue and perhaps not from
a possible CNS injury as suggested [13, 14], it becomes increasingly difficult to
make the suggested separation, especially when considering that the definition of
WAD is based on the trauma rather than the lesion [15, 16].
The proposed pathomechanics of whiplash injury have evolved from an injury
model of rapid hyperextension of the cervical spine, creating large sagittal-plane
angular displacements, to the current model of injury resulting from the body’s
inertial response, causing the head-neck complex to undergo large amounts of dis-
placement without being exposed to any direct impact. For example, during a rear-
end impact, the occupant’s torso is rapidly carried forward as it is contacted by the
forward-moving vehicle’s seat. This movement is responsible for the development
of an ephemeral “S-shaped” cervical curve, forcing the cervical spine into abnor-
mal, nonphysiological motion of lower segmental extension and upper segmental
flexion. As a result of this nonphysiological motion, energy is stored in the elastic
components of the cervical spine, followed by an abrupt release of energy and sub-
sequent forward thrust of the head and neck (acceleration/deceleration of the
head/neck and torso). The consequences of this energy release could potentially
impact and injure any number of anatomical tissues in the cervical spine (interver-
tebral disks, joint capsules, ligaments, facet joints, muscles, and nerve tissues). This
abnormal motion has been shown to produce elongation and subfailure strain of the
facet capsular ligaments at the C6–C7 level during the initial “S-shaped” phase
(between 0 and 75 ms). Maximum head and neck displacement is observed during
the second phase of this abnormal motion (100 ms), and all cervical segmental lev-
els are extended. Furthermore, the occurrence of facet joint spearing of the superior
articular facet onto the compromised inferior articular facet and stretching of the
anterior ligamentous tissues contributes to the mechanism of injury and may explain
the nature of painful symptoms following whiplash [17].
There are a variety of unique injuries involving the cervical facet joints, spinal
dorsal ganglia (DRG), ligamentous tissues, and intervertebral disks. In cervical
facet joint injuries, these include the occurrence of hemarthroses, capsular tears,
9 Pathophysiology of Whiplash-Associated Disorders: Theories and Controversies 91
articular cartilage damage, joint fractures, and capsular rupture. Moreover, the facet
joints are abundantly innervated with A-delta and C-nerve fibers that operate at a
high threshold and may become sensitized or excited by local pressure changes,
capsular stretching, and naturally occurring proinflammatory agents (substance P,
phospholipase A, and interleukin 1β). The anatomical locations of the dorsal root
ganglion (DRG) and nerve roots render them vulnerable to excessive stretching and
injury during rapid acceleration/deceleration (“S-shaped” curve) or lateral bending
of the neck. Each segmental cervical DRG contains distinct nerve fibers responsible
for relaying specific information to the spinal cord and brain (e.g., proprioception,
pain, and temperature). DRG compression and soft tissue changes, which remain
largely undetected with conventional radiography, may contribute to adaptation in
the overall functioning of the cervical DRG and may predispose an individual to
abnormal, centrally mediated pain processing [18, 19].
It should be also pointed out that peripheral nerve lesions have been demon-
strated to occasionally produce motor disturbance and such adverse symptoms as
Parkinsonism, tremor, and dystonia [20, 21].
It has been shown potentially injurious musculotendinous strains of the sterno-
cleidomastoid muscle during whiplash injury and larger strains in the superficial
posterior neck muscles (semispinalis and splenius capitis and upper trapezius) dur-
ing rear-end impacts.
Therefore, while evidence exists to suggest the occurrence of muscle strain dur-
ing the eccentric phase of a rear-impact whiplash, it is currently unknown if differ-
ential responses are noted in the deep versus superficial extensor muscles. Future
research is warranted to investigate this question.
The lack of in vivo, gold-standard diagnostic tests aimed at specifically identify-
ing these proposed lesions appears to be due to the poor sensitivity of current radio-
logical imaging techniques. While evidence from in vitro studies indicates that the
injury can damage any number of anatomical structures in the cervical spine at any
segmental level, it is largely unknown if these lesions occur either in combination
or are independent of one another.
9.2.2 Central Nervous System Lesions
Patients commonly report symptoms such as irritability, emotional lability, insom-

nia, and difficulties with concentration after cervical spine hyperextension injury.
Cerebral symptoms after a neck sprain have been taken as an indication of neurotic
personality; however, the acceleration forces could produce significant intracranial
injury in the absence of direct head impact, and this is provided by neuropsycho-
logical tests which have consistently shown deficits in attention, concentration, and
memory consistent with injury to frontobasal and upper brain stem structures. These
deficits have been found both early and late after the injury. Structural lesions have,
however, been more elusive. Examinations with MRI and brainstem auditory
evoked potentials, sensitive investigations for brainstem lesions, have been
normal.
Neuroimaging techniques have failed to report visible structural damage after

whiplash injuries [cf Chap. 6]. This has been taken as evidence that whiplash trauma
does not produce significant cerebral lesions. The same may be said for mild brain
injuries [22]. The cervical trauma resulting from a whiplash injury often coincides
with a significant acceleration-deceleration of or even direct impact to the head,
which can be suspected to produce mild traumatic brain injuries. Furthermore, some
of the symptoms of WAD are similar or identical to those of mild traumatic brain
injuries and post-concussional syndromes. For example, attention deficits, concen-
tration disturbances, fatigue, and sleep disturbances as well as depression, anxiety,
and pain are common findings [23]. Diffuse axonal injury produced by shear forces
generated during acceleration-deceleration of the nervous tissue is considered to
constitute the primary pathophysiologic cause of traumatic brain injuries especially
to the parasagittal white matter [24, 25].
Decreased attention is a major result of mild traumatic brain injuries and is
also considered to cause concomitant cognitive deficits [26]. The decreased
attentiveness may remain for a longer period depending upon the age of the
patient and may not be completely restored even after years. Especially demand-
ing work situations, fatigue, or other disorders may unveil the imperfect recov-
ery. An alternative pathophysiologic mechanism causing central nervous lesions
in whiplash injuries has been suggested by Portnoy [27] in the monkey and
Svensson in the pig [28]. During the intense deceleration of the head, there is a
fast and short rise of the intracranial and also intraspinal cerebrospinal fluid pres-
sure, approaching values as high as 150 mmHg. The authors argue that such a
pressure peak may cause damage to the neural tissue and be responsible for the
concomitant symptoms. Again, the validity of the hypothesis remains to be tested
further.
9.2.3 Vestibular Lesions
Several investigators report a high frequency of abnormal central vestibular signs in

patients with whiplash injuries [29].
Complaints of dizziness and disorders of balance occur in as many as 23 % of
patients after acceleration injuries to the cervical spine. As clinical examination is
usually normal, the pathological basis for these symptoms is unclear and has vari-
ously been attributed to vertebral artery or inner ear or disturbance of the neck right-
ing reflex induced by paraspinal muscle spasm. Objective evidence of vestibular
involvement has been demonstrated by the correlation of symptoms with electro-
nystagmograms: some patients with dizziness after neck injury show latent nystag-
mus, abnormal caloric tests, and abnormal rotatory tests.
The acceleration forces could cause significant damage to the delicate middle
and inner ear structures, and faulty inner ear function leads to ineffective muscular
control of balance and erect posture. Perilymph fistulae requiring surgery were
found in few patients.
9 Pathophysiology of Whiplash-Associated Disorders: Theories and Controversies 93
Conclusions
There is no consensus about the pathophysiological mechanisms of whiplash or
WAD. There is no consensus about the pathophysiological mechanism of whip-
lash or WAD. It seems possible that the combination of CNS lesions and soft
tissue or peripheral neural lesions might enhance each other or coincide to pro-
duce the diverse set of symptoms that one might encounter in these patients.
Furthermore, a disturbed attention span may result in different sets of cognitive
impairments, concentration deficits, and fatigue. Long standing pain may also
trigger psychiatric conditions. WAD per se seems to evoke psychiatric conditions
such as anxiety and depression. Although it is unclear to what extent this is due
to the lesion itself or secondary to other symptoms, these psychiatric impair-
ments may themselves contribute to the distress of the patient.
The possibilities of malingering ones’ symptoms to receive medicolegal ben-
efits have not been discussed here.
Improvements in medical imaging techniques may allow better definition of
these specific injuries and the development of more appropriate treatment.
At the present we have to conclude that we do not have a specific unifying
explanation of WAD.
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The Contribution of Posturology
in Whiplash Injuries 10
P.M. Gagey, D.C. Alpini, and E. Brunetta
Posturology studies disorders of the central nervous system (CNS), thanks to

the categories of space and time. Indeed, at the end of the nineteenth century,
Jean-Marie Charcot and the Salpetriêre’s French school suggested to isolate the
disorders of the CNS that were caused by a lesion—i.e., belonged to a spatial,
anatomic category. That fertile suggestion led to the foundation of neurology.
Jean-Bernard Baron [1] was the first doctor, as far as we know, to observe the
“butterfly effect” during his experiences (1955) on the regulation of the postural
tonic activity. Butterfly effect has been described by Lorentz [2]: “A butterfly beats
his wings in Brazil and a tornado is released to Texas” to say that the logic of the
postural control systems make a minor modification of one of their parameters that
could bring consequences without proportionality between causes and effects.
Following and continuing those works, many doctors in southern Europe started to
study disorders of the central nervous system whose logical structure is based not
on an anatomical lesion but on the chaotic logic of chained temporal series. Such
studies—particularly vigorous in the field of postural control—constitute
posturology.
The fundamental concept of posturology is the “Fine Postural Control System”
to say that postural control adapts itself to the various behaviors of man: if he is
walking or quiet standing, mechanisms implied in his postural control are not the
same [3, 4].
P.M. Gagey (*)

Institut de Posturologie, Av. de Corbera 4, Paris, France
e-mail: pmgagey@club-internet.fr
D.C. Alpini
Milan, Italy
E. Brunetta
Private Dentist, Conegliano (TV), Italy
e-mail: elvio.brunetta@fastwebnet.it

96 P.M. Gagey et al.
Human being, indeed, controls his position in his environment according to a

fundamental operational scheme, common to all behaviors:
• He anticipates his posture according to what he decides to do.
• He controls it by the different inputs of his postural control system.
• He corrects it by muscle activity, either phasic or tonic.
This global scheme may be modulated. Adaptation of postural control to quiet
standing, specified by this behavior, is characterized by:
• A predominance of tonic muscle activity
• A discontinuity of the functioning of some system inputs
• A predominance of feedback loops
Whiplash injuries impact strongly on the “Fine Postural Control System” both
on tonic muscle activity and on sensorial feedbacks. Whiplash leads, in the great
majority of patients, to the so-called disharmonious postural syndrome typically
characterized by the absence of proportionality between the mechanical forces of
the impact and the consequent effects on static and dynamic postural control.
10.1 Disharmonious Postural Syndrome
Clinical theory suggests that altered alignment of the shoulder girdle has the poten-
tial to create or sustain symptomatic mechanical dysfunction in the cervical and
thoracic spine. The alignment of the shoulder girdle is described by two clavicle
rotations, i.e., elevation and retraction, and by three scapular rotations, i.e., upward
rotation, internal rotation, and anterior tilt. The search for an abnormal postural
tonic asymmetry forms the basis of the clinical postural examination. This asym-
metry at the level of the axial musculature obeys to the laws of spinal movement as
stated by Lowett (1907) (cited by Fryette [5]):
lateral inclination of the spine of the subject standing up is accompanied by a contralateral

rotation of the lumbar and dorsal vertebrae. This finding is easily perceived by gently plac-
ing one’s hands on the patient’s iliac wings and scapulae, while he leans sidewards.
Distal musculature can be explored by means of Fukuda’s stepping test [6]

followed by measurement of neck reflex gains [7].
When the muscle tone is abnormally asymmetrical, we can speak of a “postural
syndrome”: it is said to be “harmonious” when the hypertonicity is crossed between
the axial and distal musculatures; in the opposite case, the postural syndrome is said
to be “disharmonious.” Barré’s “vertical” provides a visual summary of these
postural syndrome analyses (Fig. 10.1).
The overwhelming majority of whiplash victims present a disharmonious
postural syndrome; this surprisingly high incidence of disharmonious postural
syndrome following whiplash is statistically significant.
Uemura and Cohen [8] showed that by localized destruction of the vestibular
nuclei in the monkey, it was possible to induce harmonious or disharmonious
postural syndromes depending upon the level of the lesion. However, it is difficult
10 The Contribution of Posturology in Whiplash Injuries 97
Fig. 10.1 Harmonious and

disharmonious postural L R L R
syndromes. On the left, in
harmonious syndrome, the
hypertonicity of the axial and
distal muscles is crossed. On
the right, in disharmonious
postural syndrome, the
hypertonicity of the axial and
distal muscles is homolateral
(From Ref. [7])
to imagine that whiplash systematically produces a lesion of the vestibular nuclei

and even more difficult to think that such a lesion would always occur at the same
site. Thus, the meaning of a disharmonious postural syndrome must be sought else-
where. A clear-cut asymmetry of the electric activity of the neck muscles almost
always exists following whiplash [9], and this does not seem strange when we
remember the incidence of cervical articulation lesions caused by this type of
trauma. The muscles contract to mitigate the consequences of rupturing ligaments.
The postural importance of these cervical muscles could be showed by stabilomet-
ric recordings of these patients: significant asymmetry of the areas of the statokine-
sigrams appears between the recordings made with the head turned to the right and
then to the left (Fig. 10.2).
Helgadottir et al. [10] confirmed the postural asymmetry in neck pain and WAD.
Elevation and retraction have been assessed through a three-dimensional device
measured clavicle and scapular orientation, and cervical and thoracic alignment in
patients with insidious onset neck pain (IONP)and whiplash-associated disorder
(WAD). An asymptomatic control group was selected for baseline measurements.
The symptomatic groups revealed a significantly reduced clavicle retraction and
Left rotation Right rotation

Y Y
o o
X x
1 cm 1 cm
Statokinesigram Statokinesigram
Fig. 10.2 Stabilometric recordings with the head turned to the left and the right. On the left, the
subject’s head was turned to the left during the recording session: the area of the statokinesigram
is 2.092 mm2. On the right, the subject’s head was rotated to the right during the recording session:
the area of the statokinesigram is 867 mm2. The ration of the areas or the cervical quotient is sta-
tistically significant: 2.41 (p < 0.05)
scapular upward rotation as well as decreased cranial angle. A difference was found
between the symptomatic groups on the left side, whereas the WAD group revealed
an increased scapular anterior tilt and the IONP group a decreased clavicle eleva-
tion. These changes may be an important mechanism for maintenance and
recurrence or exacerbation of symptoms in patients with neck pain.
Furthermore, whiplash-associated posture modification in the sagittal plane has
been studied by Johansson et al. [11] that investigated whether a kyphotic deformity
of the cervical spine, as opposed to a straight or a lordotic spine, was associated with
the symptoms at baseline and with the prognosis 1 year following a whiplash injury.
MRI was performed in 171 subjects about 10 days after the accident, and 104 par-
ticipated in the pain recording at 1-year follow-up. It was demonstrated that pos-
tures as seen on MRI can be reliably categorized and that a straight spine is the most
frequent appearance of the cervical spine in supine MRI. In relation to symptoms, it
was seen that a kyphotic deformity was associated with reporting the highest inten-
sities of headache at baseline, but not with an increased risk of long-lasting neck
pain or headache. According to the authors, a kyphotic deformity was not signifi-
cantly associated with chronic whiplash-associated pain and that pain should not be
ascribed to a straight spine on MRI.
10.2 The Fundamental Oscillation at 0.2 Hz
The ability to maintain balance is diminished in patients suffering from a whiplash

injury. Stabilometry is a widely accepted method to document the impact of
whiplash on static postural control.
Recently Madeleine et al. [12] investigated the variability of postural control in
patients with chronic whiplash injury analyzing stabilometric recordings from 11
10
Attenuation (dB)
20
30
40
50
60
70
0.15 0.25 0.5 1 1 1.5 2 2.5
Frequencies (Hz)
Fig. 10.3 Fourier’s transform of the stabilometric signals of a whiplash victim. The fundamental
oscillation GI is evident, clearly separated, at a frequency band of about 0.2 Hz (From Ref. [7])
whiplash patients and sex- and age-matched asymptomatic healthy volunteers.

Spatial-temporal changes of the center of pressure displacement were analyzed to
assess the amplitude and structure of postural variability by computing, respec-
tively, the standard deviation/coefficient of variation and sample entropy/fractal
dimension of the time series. The amplitude of variability of the center of pressure
was larger among whiplash patients compared with controls (P < 0.001), while frac-
tal dimension was lower (P < 0.001). They showed that sample entropy increased
with both eyes closed and a simple dual task compared with eyes open (P < 0.05).
The analysis of postural control dynamics revealed increased amplitude of postural
variability and decreased signal dimensionality related to the deficit in postural sta-
bility found in whiplash patients.
A specific contribution to comprehension of the complex phenomena that sub-
serve postural control is the frequency analysis of the stabilometric signals. Using
the Fourier transform in WAD patients, a fundamental oscillation around 0.2 Hz
(Fig. 10.3) is frequently observed. This fundamental oscillation at 0.2 Hz appears
equally on recordings made with the eyes open or closed.
This 0.2 Hz fundamental oscillation must not be confused with the fundamental
oscillation at 0.3 Hz described by Taguchi [13]. The 0.3 Hz frequency corresponds
to the resonance frequency of the inverted human pendulum that appears during
dysregulations of the fine postural control system of which it is sometimes the only
stabilometric witness. This fundamental oscillation simply demonstrates that the
postural system is no longer able to damp out this resonance frequency of the human
pendulum.
The 0.2 Hz fundamental oscillation has a completely different significance.
Patients suffering from rachis pain is characterized by a peak at the frequency of
0.2 Hz, when the mean power spectrum is compared to a population of normal
subjects [7]. However, this fundamental oscillation is not pathognomonic of a spine
disorder; it has another origin.
The respiration rhythm is situated in this frequency band of 0.2 Hz; it does not
appear or appears only slightly on the stabilograms of normal standing subjects [4,
14]. Gurfinkel and Elner [15] suggest the possibility of a postural adjustment in
preparation of the act of breathing that corrects in advance the postural perturba-
tions resulting from movements of the thoracic cage.
It seems important to emphasize the incidence of the appearance of this respira-
tory rhythm on the stabilograms of subjects with a spine dysfunction, because Tardy
[16] showed very close relationships between the static spinal musculature and the
muscles involved in respiration.
Postural control in WAD is disturbed even if subjects are seated as shown by
Cote et al. [17] that investigated kinematic and electromyographic postural stabili-
zation patterns in individuals with chronic WAD. Ten individuals with WAD and an
age- and gender-matched group of healthy individuals were exposed to sudden
forward and backward support surface translations while they were seated. Neck
and trunk muscle activity and angular displacements as well as centers of mass
(COMs) linear displacements at four levels of the head and trunk were computed.
The displacement onset of the combined head, arms, and trunk COM was signifi-
cantly delayed in persons with WAD. However, their peak trunk angles were
smaller and were reached sooner. In the WAD group, the activation onset of the
lumbar erector spinae was less affected by perturbation direction, and the sterno-
cleidomastoid muscle, a neck flexor, showed a trend towards being activated later,
compared to the healthy group. These results suggest that individuals with WAD
may alter stretch reflex threshold and/or elicit a learned response for pain avoidance
that may be direction specific. Such findings highlight the importance of assessing
both spatial and temporal characteristics across different levels of the spinal
musculoskeletal system to evaluate multidirectional postural responses in WAD
individuals.
10.3 Asymmetry of the Activity of the Neck Muscles
Neck muscles are responsible for directing the head and for maintaining its posture.
These functions are accomplished statically and dynamically, using various levels
of contraction, by 22 muscle pairs that connect the head with the cervical spine and
shoulder girdle. Optimal integration of this muscular complex is essential for nor-
mal functioning of the head-neck complex, whereas compromising it may result in
associated pain and/or disability. Although assessing neck musculature may be con-
ducted using imaging (ultrasound, computed tomography, magnetic resonance
imaging) and electromyographic studies, from the functional point of view, the rel-
evant parameter(s) refers to the mechanical expression of muscle function which is
invariably reflected by the ability of neck muscles to develop force (strength) and to
sustain it (endurance).
Fig. 10.4 Electromyograph (EMG) of neck muscles. EMG of the superior heads of the right and
left trapezius muscles of a whiplash victim with his head in the normal position. The asymmetry
of the tracings is obvious (From Ref. [7])
Manual muscle testing (MMT) [18] could be used for assessing sagittal and
transverse plane strength. Testing is conducted with the patient at the prone (for
extension) and supine (for flexion and rotation). Strength could be rated accord-
ing to the MMT scale with grade 3 being equivalent to resisting gravity. Given the
specific role of cervical muscles, preserving grade 3 would, in most cases, be
sufficient for most functional activities since in these test positions the moment
developed by the muscles is already in excess of the strength level required for
normal activities. On the other hand, MMT is of a low validity when strength is
to be rated as grade 4 or 5. Moreover, unlike the frontal plane, where the direc-
tional forces—lateral flexion to the right and to the left—are supposed to be sym-
metric and, hence, can serve reciprocally for comparison, such is not the case
with flexion and extension as each depends largely on distinct muscle groups.
Thus, MMT is not a recommended means for assessing cervical strength above
grade 3.
Boquet and Boismare [19] studied comparatively the electromyograph (EMG) of
the superior heads of the trapezius muscles, left and right. In whiplash victims, they
almost always find marked asymmetry of these EMGs, with the patient’s head in
either the normal position (Fig. 10.4) or between positions with the head turned to
the left and to the right (Fig. 10.5).
What is most remarkable on the EMG tracings of these patients is not only the
asymmetry but also the amplitude of electrical activity.
Boquet noted signs of increased levels of vigilance, emotionalism, and basic
anxiety in these patients. All whiplash victims do not necessarily have postural
disorders. A supplementary factor is required which Boquet and Boismare link to
this hypervigilance, that is, anxious individuals very often have neck pains and
they blame it on early arthritis, but wrongly so, because one sees people with
arthritis sufficiently severe to generate cracking sounds without any complain and
contractures, but are calm individuals. This clinical contrast underlines the
100 ms
200 µV
Fig. 10.5 Electromyograph (EMG) of neck muscles. EMG of the superior heads of the right
(uneven numbers) and left (even numbers) trapezius muscles. 1–2: head in the normal position;
3–4: head turned to the right; 5–6: head turned to the left. The asymmetry appears when the head
is rotated towards the right (From Ref. [7])
increased reactivity of neck neuromuscular spindles when the vigilance level is

heightened [20]. This brings to mind the fundamental studies that demonstrated the
noradrenergic innervation of the neuromuscular spindles and, more generally, the
influence of the autonomous nervous system on the postural system. Ehrenborg
and Archenholtz [21] showed that there is no support for the effectiveness of
surface EMG biofeedback training as a supplement to an interdisciplinary rehabili-
tation program for people with long-lasting pain after whiplash.
10.4 Treatment
Treatment of post-traumatic cervical syndrome by strictly postural techniques

(optical prisms, stimulation soles) has been a failure. But clinical posturology has
taught us that, with every failure of postural treatments, a poorly understood lesion
Normal
Sprain
Fig. 10.6 Posterior walls, normal and after cervical sprain
must be sought. This is indeed the case, well established today, for mandibular
lesions responsible for craniomandibular dysfunctions; we now know that the latter
must be treated prior to initiating any postural therapy. This is also true for irritative
lesions of plantar pressure points that are able to generate distant postural dysfunc-
tion; these lesions must be dealt with first. This hierarchy of treatments is easily
explained: prisms and stimulation soles can only modify sensory integration.
Addressing the lesion takes precedence over the subtleties of improving sensory
integration.
Nowadays, lesions of the cervical spine after whiplash are far from always being
poorly understood; medical imaging techniques have made enormous progress.
Even before the era of computed tomography scanners and magnetic resonance
imaging, Gentaz et al. [22], by multiplying the dynamic projections for radiography
of the cervical spine, had detected obvious signs of cervical sprain, e.g., rupture of
the continuity of the posterior wall of the vertebral bodies (Fig. 10.6) or overlapping
of posterior articulations.
Normally, the posterior faces of the vertebral bodies remain perfectly aligned,
even during hyperflexion and hyperextension of the neck. When a steplike shift
appears in this posterior wall (between C3 and C4 in the drawing on the right of
Fig. 10.6), a ligament has been torn, the neck sprained. These shifts usually only
appear in dynamic positions, in this case, hyperextension.
Discovery of a cervical lesion subsequent to whiplash seems so important that
we are tempted to say that no diagnosis of post-traumatic cervical syndrome can be
made in its absence, especially when the whiplash is not recent. As long as the
lesion is not found, it must be sought with perseverance.
If, despite the multiplication of tests, the lesion is not seen, the diagnosis should
remain highly suspect. The neck is the privileged site of expression of all sorts of
“distant” pathologies, such as oculomotor disorders, strabism, torticollis, occlusion
pathologies, spinal, and even plantar disorders—that have nothing to do with whip-
lash. The cervical spine is a trap for the clinician.
It is useless to apply postural techniques to treat a whiplash victim with a cervical
sprain. Therapy of the lesion takes precedence over attempts to manipulate sensory
integration.
In contrast, Boquet and Boismare [19] insist upon the necessity to treat from the
start the excessive anxiety, translated as permanent neurectasia, of these patients.
The recommended therapeutic strategy is myoresolutive and sedative. The treat-
ment starts pharmacologically with a diazepam (20 mg/ml) drip, in combination
with 1-and f3-blockers that reduce the activity of the autonomous nervous system.
The dosages are adjusted until the desired levels of vigilance and muscular tonus are
obtained for each subject. Once the patient is “relaxed,” work on the neck.
Conclusion
For more than 100 years, since the studies of Longet [23], we have known that
the neck muscles are involved in postural control and we confirm this knowledge
every day in whiplash victims. However, over the past few years, our attention
has been drawn towards the overall level of vigilance of these patients that must
be taken into account before starting therapy.
We are also better able to explore the traps posed by the cervical spine, where
numerous postural tonic pathologies can express themselves without any local
lesion. These observations lead us to insist upon searching signs of cervical
sprain using all available means of medical imaging before settling on a diagno-
sis of whiplash.
The discovery of a cervical lesion is extremely important for determining the
therapeutic strategy—it formally counter indicates the use of any postural
techniques.
References
1. Baron JB (1955) Muscles moteurs oculaires, attitude et comportement locomoteur des
vertébrés. Doctoral thesis in Science, Université de Paris
2. Lorenz EN (1993) The essence of chaos. UCL Press, London
3. Gagey PM, Martinerie J, Pezard L, Benaim C (1998) L’équilibre statique est contô1é par un
système dynamique non-linéaire. Acta Otolaryngol 115:161–168
4. Gagey PM, Toupet M (1997) Le rythme ventilatoire apparaît sur les stabilogrammes en cas de
pathologie du système vestibulaire ou proprioceptif. In: Lacour M, Gagey PM, Weber B (eds)
Posture et Environnement. Sauramps, Montpellier, pp 11–28
5. Fryette HH (1978) Principes des techniques ostéopathiques. Maloine, Paris
6. Fukuda T (1959) The stepping test: two phases of the labyrinthine reflex. Acta Otolaryngol
50:95–108
7. Gagey PM, Weber B (1995) Posturologie; régulations et dérèglements de la station debout.

Masson, Paris
8. Uemura T, Cohen B (1973) Effects of vestibular nuclei lesions on vestibulo-ocular reflexes and
posture in monkeys. Acta Otolaryngol Suppl 315:1–71
9. Gagey PM (1986) Postural disorders among workers on building sites. In: Bles W, Brandt T
(eds) Disorders of posture and gait. Elsevier, Amsterdam
10. Helgadottir H, Kristjansson E, Mottram S, Karduna A, Jonsson H Jr (2011) Altered alignment
of the shoulder girdle and cervical spine in patients with insidious onset neck pain and
whiplash-associated disorder. J Appl Biomech 27(3):181–191
11. Johansson MP, Baann Liane MS, Bendix T, Kasch H, Kongsted A (2011) Does cervical kypho-
sis relate to symptoms following whiplash injury? Man Ther 16(4):378–383. Epub 2011 Feb 3
12. Madeleine P, Nielsen M, Arendt-Nielsen L (2011) Characterization of postural control deficit
in whiplash patients by means of linear and nonlinear analyses—a pilot study. J Electromyogr
Kinesiol 21(2):291–297. Epub 2010 June 16
13. Taguchi K (1978) Spectral analysis of the movement of the center of gravity in vertiginous and
ataxic patients. Agressologie 19B:69–70
14. Bouisset S, Duchene JL (1994) Is body balance more perturbed by respiration in seating thaò
in standing posture? Neuroreport 5:957–960
15. Gurfinkel VS, Elner AM (1968) The relation of stability in a vertical posture to respiration in
focal cerebral lesions of different etiology. Neuropathol Psychiatry 58:1014–1018 (in Russian)
16. Tardy D (1992) Systèmes moteurs posturaux du tronc, vieillissement, déclin. Crit Posturol
52:1–9
17. Côté JN, Patenaude I, St-Onge N, Fung J (2009) Whiplash-associated disorders affect postural
reactions to antero-posterior support surface translations during sitting. Gait Posture
29(4):603–611. Epub 2009 Feb 7
18. Dvir Z, Prushansky T (2008) Cervical muscles strength testing methods and clinical implica-
tions. J Manipulative Physiol Ther 31(7):518–524
19. Boquet J, Boismare F (1982) Étude physiopathologique du syndrome cervical post-
traumatique: ROie du tonus végétatif. Rev Fr Dommage Corpor 8:397–410; Hunt CC, Jame L,
Laporte Y (1982) Effects of stimulating the lumbar sympathetic trunk on cat hindlimb muscle
spindles. Arch Ital Biol 120:371–384
20. Grassi C, Perin F, Artusio E, Passatore M (1993) Modulation of the jaw jerk reflex by the
sympathetic nervous system. Arch Ital Biol 131:213–226
21. Ehrenborg C, Archenholtz B (2010) Is surface EMG biofeedback an effective training method
for persons with neck and shoulder complaints after whiplash-associated disorders concerning
activities of daily living and pain -a randomized controlled trial. Clin Rehabil 24(8):715–726.
Epub 2010 June 18
22. Gentaz R, Gagey PM, Goumot J, Rouquet Y, Baron JB (1975) La radiographie du rachis
cervical au cours du syndrome post-commotionnei. Agressologie 16A:33–46
23. Longet FA (1845) Sur les troubles qui surviennent dans l’équilibration, la station et la locomo-
tion des animaux après la section des parties molles de la nuque. Gaz Med Paris 13:565–567
Whiplash-Associated Autonomic
Effects 11
R. Boniver, D.C. Alpini, and G. Brugnoni
11.1 Introduction
There is some evidence available indicating that autonomic disturbances are present
in chronic WAD. Impaired peripheral vasoconstrictor responses have been
demonstrated in both acute and chronic whiplash, but the relationship of these
changes to the clinical presentation of whiplash or outcomes following injury is not
clear. Gaab et al. [1] have shown reduced reactivity of the hypothalamic–pituitary–
adrenal axis, a closely interacting system to the autonomic system, in a small sam-
ple of participants with chronic WAD. Autonomic nervous system dysfunction has
been found to be present in other painful musculoskeletal conditions such as chronic
low back pain, fibromyalgia, and cervicobrachialgia.
Individuals with posttraumatic stress disorder (PTSD) also show evidence of
autonomic and hypothalamic–pituitary–adrenal dysfunction [2–5] which may have
some relevance for WAD where recently it was shown that a significant proportion
of injured people also have a probable diagnosis of PTSD.
There are obvious links between the cervical proprioceptors and the musculo-
skeletal system, but links to the autonomic nervous, vestibular, and visual systems
and influence on pain modulation although important under a clinical point view are
not yet well underlined.
R. Boniver (*)
Department of Otolaryngology, Université de Liège, Rue de Bruxelles 21,
B-4800 Verviers, Belgium
e-mail: r.boniver@skynet.be
D.C. Alpini
Milan, Italy
G. Brugnoni
Italian Academy of Manual Medicine, Italian Institute for Auxology, Milan, Italy

108 R. Boniver et al.
Dizziness is one of the most frequent complaints in those with persistent pain
after a whiplash trauma, and it is often associated with postural control distur-
bances. Postural control may have potential to alter other systems and affect pain
and should be considered as one of the processes that might influence the transition
to chronicity after a whiplash trauma.
According to Trevalen [6, 7] transition from acute to chronic WAD is due to
involvement of the autonomic system with special regard to cervical part of it.
Besides its well-known action on muscle blood flow, the sympathetic nervous
system (SNS) is able to affect the contractility of muscle fibers, to modulate the
proprioceptive information arising from the muscle spindle receptors, and, under
certain conditions, to modulate nociceptive information. Furthermore, the activity
of the SNS itself is in turn affected by muscle conditions, such as its current state of
activity, fatigue, and pain signals originating in the muscle.
The thesis of Trevalen et al. is sustained by the review of Passatore and Roatta
[8] that focuses on the actions exerted by the sympathetic system at muscle level in
WAD, with particular emphasis being devoted to sensorimotor symptoms.
The autonomic genesis of dizziness that could lead to postural disorders and
then to chronic pain was sustained by Barrè [9] in 1924. He described the so-
called posterior cervical sympathetic syndrome and proposed that cervical
lesions might irritate the sympathetic vertebral plexus and result in a decreased
blood flow to the labyrinth due to constriction of the internal auditory artery.
Although numerous clinical reports of Barré syndrome have been published, few
objective data exist to support an association between episodic vertigo and cervi-
cal sympathetic dysfunction. Since intracranial circulation is autoregulated inde-
pendently of cervical sympathetic control, it is unlikely that lesions in the
vertebro-sympathetic plexus could produce focal constriction of the vasculature
to the inner ear.
Hinoki, first in 1971 [10] and in detail in 1985 [11], proposed a hypothesis in
which the hypothalamus takes a fundamental place to explain vertigo due to
whiplash injury.
11.2 The Autonomic Nervous System
The autonomic nervous system (ANS) is the part of the nervous system, both
afferent and efferent, that innervates various body systems that are not under
voluntary control. These include the constriction and dilation of blood vessels, the
activity of the viscera, and the secretion of glands (secretomotor fibers), and assist
the endocrine system to maintain a constant internal environment (homeostasis).
The afferent neurons have their peripheral receptors in the wall of viscera
and blood vessels and their cell bodies in the dorsal root ganglia or cranial nerve
ganglia. Their central processes end in the dorsal gray column of the spinal cord or
the brain stem.
The efferent neurons supply the smooth muscles in the wall of hollow viscera
and blood vessels. They can be either excitatory or inhibitory.
11 Whiplash-Associated Autonomic Effects 109
The efferent pathway is made up of two neurons:

1. A preganglionic neuron (myelinated), located in the spinal cord or brain stem,
synapsing with
2. Postganglionic neuron(s) (unmyelinated) in an autonomic ganglion
Functionally, the ANS is divided into sympathetic and parasympathetic
systems.
The sympathetic nervous system (SNS) prepares the body for “fright, fight, or
flight.” It increases the heart rate and ventricular contraction, dilates the blood
vessels in skeletal muscles, constricts blood vessels in the skin and guts, increases
blood sugar level, stimulates sweating, dilates the pupils, and inhibits activities of
the guts and gastric secretion.
The sympathetic outflow from the central nervous system (CNS) is thoracolum-
bar, emerging from the spinal cord segments T1–L3. The sympathetic ganglia form
a string of beads called the sympathetic trunk, lying on either side of the vertebral
bodies. The two trunks extend from C1 to the level of the coccyx where they unite
at the midline at the ganglion impar.
The preganglionic fibers leave the spinal cord with the ventral root of the
corresponding spinal nerve and pass to the corresponding sympathetic ganglion via
the white ramus communicans (white because the fibers are myelinated). In that
ganglion, they may synapse with postganglionic fibers which leave the sympathetic
trunk in the gray ramus communicans, rejoin the same ventral ramus, then are
distributed to the target organs (smooth muscles of blood vessels, sweat glands…),
travel up or down the trunk to synapse with postganglionic fibers in other ganglia
(e.g., cervical, lumbar, sacral, which do not receive direct rami communicantes
from the cervical, lower lumbar, or sacral segments), or pass through the ganglion
without relay to synapse in prevertebral ganglion (e.g., celiac ganglion, known to
lay people as “solar plexus”).
The parasympathetic nervous system (PNS) is more active at rest, having in
general anabolic effects. For example, it slows down the heart rate, constricts the
pupils, and increases gastric secretion and intestinal motility.
The parasympathetic system outflow is craniosacral, emerging from the
oculomotor, facial, glossopharyngeal, and vagus nerves and the spinal cord seg-
ments S2, S3, and S4. These fibers travel in the branches of sacral nerves S2–S4
(nervi erigentes) to the pelvic viscera.
The parasympathetic system supplies the heart, glands, and smooth muscles of
the viscera, not the sweat glands, blood vessels, or erector pilorum muscles.
11.3 The Hypothalamus
The hypothalamus is unquestionably of great significance both phylogenetically

and anthropologically. It plays striking roles in many aspects of mammalian physi-
ology. It undoubtedly contains integrative mechanisms which, in addition to their
effect on behavior patterns, also aid in regulating the basic life functions of the
organism. However, this integration is apparently carried out through its
relationship with other parts of the nervous system, including the so-called higher
levels, as well as through the endocrine system.
It is in this field of interrelationship that some of the most pressing problems lie.
It must be appreciated that while this interesting region of the brain is only part of a
system of complex circuits, it is an extremely important link in these circuits and is
so strategically placed that its derangement may have profound effects.
It is important that the hypothalamus be regarded as part of a series of complex
neural circuits involving the brain stem, cerebral hemisphere, and other parts of
the diencephalon. These circuits are poorly understood, but evidence for rich con-
nections with septal, subcallosal, preoptic, and frontotemporal areas has been
offered. The hypothalamus is considered to be the most rostral portion of the retic-
ular formation and similarly is poorly differentiated with the exception of the mag-
nocellular neurosecretory system. The hypothalamus is also the most caudal aspect
of the limbic system and thus the brain region through which limbic system output
comes to control autonomic and endocrine function.
The paraventricular nucleus of the hypothalamus (PVN) is one of the most vas-
cularized areas of the brain. The PVN distinguishes itself from other hypothalamic
nuclei in that it plays the dominant role in neuronally coupling autonomic, endo-
crine, and somatomotor responses to environmental stressors. It accomplishes this
through a rich network of innervation from the forebrain, limbic system, other
hypothalamic nuclei, and brain stem autonomic centers such as the nucleus of the
solitary tract and the dorsal vagal complex. PVN innervates the median eminence,
pituitary, brain stem nuclei, and spinal cord.
Concentrations in epinephrine (EPI) in the paraventricular nucleus in human
hypothalamus are rather high [12]. If stressful motion were shown to lead to a sig-
nificant rise in EPI and norepinephrine (NE), then this rise would be different from
subject to subject and would therefore be more prominent in subjects more resistant
to motion sickness. Strangely enough, in those cases, no correlations were found
between measured levels of ACTH and EPI even though EPI exerts a stimulatory
influence on the pituitary gland’s release of ACTH. It is well known that ACTH and
smaller peptides like ACTH 4–10 reduce latency in recovery of normal sensorimo-
tor functions following unilateral labyrinthectomy.
Corticotropin-releasing factor (CRF), containing neurons, have been found in
the medial vestibular nucleus and may contribute to CRF, containing climbing
fibers shown to project from the inferior olive to the cerebellum.
11.4 Hinoki’s Hypothesis
According to Hinoki, patients with whiplash injury present with a hypertonicity of

the soft supporting tissues of the neck due to the overexcitation of the cervical
proprioceptors, which is caused by an excitation of sympathical beta-receptors in
the muscle spindles. He has demonstrated the development of granular vesicles at
the end of unmyelinated nerve fibers near the motor nerve endings of these
spindles.
Abnormal centripetal impulses arising from the injured cervical soft tissues may
ascend along the spinoreticular tract to the brain stem. Among the ascending
Somato–motor
Autonomic nervous
system
system
Hypothalamus
Cerebellum
Cuneocerebellar
Brainstem Tegmento hypothalamic
tract
reticular tract
MLF formation
Reticulo Schutz’s
spinal tract Midbrain central dorsal
Oculomotor
nuclei gray matter longitudinal
Spinoreticular
fasciculus
tract
Somato motor
Muscle cells in columna Pupilo
of eyes ventralis constrictory
center
Cervical
proprioceptors Superior cervial
Post. spinocerebellar tract
sympathetic
Muscles of trunk ganglion
and limbs Pupil
Lumbar
proprioceptors
Fig. 11.1 Connections of lumbar and cervical proprioceptors within the somatomotor system
pathways from the cervical and lumbar proprioceptors to the brain stem, the
spinoreticular tract seems to be the most important, since most of its fibers ascend
along the lateral fasciculus and the anterior column and terminate in the reticular
formation of both the medulla oblongata and the pons. However, some fibers of this
tract ascend directly to the midbrain and are connected to Deiters’ nucleus.
Furthermore, this tract changes neurons in the medulla oblongata, the pons, and
the midbrain and terminates in the superior colliculus. It is generally accepted that
the reticular formation of these parts of the brain, as well as Deiters’ nucleus and the
superior colliculus, is active in both ocular and spinal reflexes related to body equi-
librium. Among the descending paths from the brain stem, the median longitudinal
fasciculus (MLF) is important in cases of vertigo, because this tract originates in the
brain stem and is connected to both the oculomotor nuclei and the somatomotor
cells in the ventral column. The reticulospinal tract also originates in the brain stem
reticular formation of both the medulla oblongata and the pons and is connected to
the somatomotor cells in the ventral column. This tract is thought to have a close
relationship with the spinoreticular tract mentioned above. Thus, the MLF and the
reticulospinal tract seem especially important in the development of disequilibrium
because of whiplash injury. The hypothalamus must also play an important role in
producing vertigo due to whiplash injury, since most of Hinoki patients, with ver-
tigo following whiplash injury, had various autonomic symptoms, such as lacrima-
tion, abnormal sweating, and palpitation.
The cerebellum is, of course, involved in the development of this type of vertigo,
since it is closely connected to the proprioceptors of the cervical and lumbar regions
as well as to the brain stem (Fig. 11.1).
After several experiments, Hinoki further demonstrated that the abnormal

autonomic reactions in patients with whiplash injury were not due to the irritation
of the injured posterior cervical sympathetic nerves but to overstimulation of the
proprioceptor of the neck.
On the basis of their report and the known fiber connections in the central nervous
system, it may be assumed that in patients with whiplash injury, delayed pupil con-
striction in response to light is probably because of overstimulation of a sympathetic
component in the hypothalamus-brain stem system brought about by centripetal
impulses from the injured proprioceptors of the neck and waist. In addition, the
spinoreticular tract is probably involved in the conduction of these impulses, since
this tract ascends along the lateral fasciculus and the anterior column in the cervical
and lumbar cords and terminates in both the reticular formation of the brain stern
and the central gray matter of the midbrain [13].
The central gray matter of the midbrain is then connected to the hypothalamus
both through the hypothalamotegmental tract and diffuse ascending neurons. There
is evidence to support this assumption, since Hinoki found that, in patients with
delayed pupil constriction in response to light, ataxia of the eyes and body tended to
be aggravated by the subcutaneous injection of adrenaline.
Moreover, Kawamura and Oshurna [14] reported that adrenaline acts directly on
the posterior hypothalamus, an important center of the sympathetic nervous system.
Okada et al. [15] also reported that in cats the electrical activities of the short ciliary
nerves, which are involved in pupil constriction, were significantly decreased by the
injection of adrenaline. According to their explanation, overstimulation of the hypo-
thalamus induced by adrenaline suppresses the activity of the pupillo-constrictory
center of the midbrain, leading to pupil dilatation.
To summarize, the overexcitation of the arrival proprioceptors should be because
of a hypersensitivity to sympathetic stimulation, inducing central disturbances by
afferent nervous pathways at the level of brain stem, cerebellar, and hypothalamus,
affecting the oculomotor system and gait control.
More recently Hinoki’s hypothesis has been supported by Matsui et al. [16].
Authors found that abnormalities in the cervical muscles after whiplash cause auto-
nomic dystonia, leading to headache, chronic fatigue syndrome, vertigo, and dizzi-
ness. They named this group of diseases cervical neuromuscular syndrome. In their
experience treatment of the cervical muscle was effective for general whiplash-
associated malaise.
Autonomic involvement after whiplash can provoke also short-lasting unilateral
neuralgiform headache with conjunctival injection and tearing (SUNCT), a rare
headache syndrome classified among the trigeminal autonomic cephalalgias. It is
usually idiopathic, although infrequent posttraumatic forms have been described
[17]. Recently the term short-lasting unilateral headache with cranial autonomic
symptoms (SUNA) has been defined by the International Headache Society (ICHD-
2) as similar to SUNCT with less prominent or absent conjunctival injection and
lacrimation.
For this kind of posttraumatic neuralgiform headache, Choi et al. [18] proposed
greater occipital nerve (GON) block as treatment.
11.5 Chronic Pain and Fatigue in Whiplash Patient
In spite of their clear traumatic origin, whiplash-associated disorders (WAD) appear

to share many common features with other chronic pain syndromes affecting the
musculoskeletal system. These features do not only include symptoms, like type of
pain or sensory and motor dysfunctions, but possibly also some of the pathophysi-
ological mechanisms that may concur to establish the chronic pain syndrome.
Studies [19–22] show that injury produces plasticity changes of different neuronal
structures that are responsible for amplification of nociception and exaggerated pain
responses. There is consistent evidence for hypersensitivity of the central nervous
system to sensory stimulation in chronic pain after whiplash injury.
Different mechanisms underlie and coexist in the chronic whiplash condition.
Spinal cord hyperexcitability in patients with chronic pain after whiplash injury can
cause exaggerated pain following low-intensity nociceptive or innocuous peripheral
stimulation. Spinal hypersensitivity may explain pain in the absence of detectable
tissue damage.
Whiplash is a heterogeneous condition with some individuals showing features
suggestive of neuropathic pain. A predominantly neuropathic pain component is
related to a higher pain/disability level [23, 24].
Chronic pain can lead to posttraumatic stress reaction (PTSR). On the other hand
the sympathetic nervous system (SNS) could sustain a posttraumatic stress reaction
(PTSR) at least in some whiplash-injured persons. Sterling and Kenardy [25] showed
in fact that patients with persistent PTSR presented sensory hypersensitivity and
impaired peripheral vasoconstriction compared to those whose PTSR resolved and
those without PTSR. The early presence of sensory hypersensitivity was associated
with PTSR at 6 months, but this relationship was mediated by pain and disability
levels. Thus, authors showed the connections between chronic pain PTSR and SNS.
The correlation between chronicization of WAD and SNS has been investigated
also by Kalezic et al. [26] that suggested a stronger autonomic reaction in WAD than
in healthy subjects in response to dynamic loading of the jaw–neck motor system to
explain impaired endurance during chewing as previously reported in WAD. Kalezic
et al. correlated cardiovascular reactivity and EMG muscle fatigue indices, and per-
ceptions of fatigue; exhaustion and pain were assessed during standardized chewing.
More than half of the WAD subjects terminated the test prematurely due to exhaustion
and pain. In line with their hypothesis, the chewing evoked an increased autonomic
response in WAD exhibited as a higher increase in heart rate as compared to controls
indicating pronounced vulnerability to dynamic loading of the jaw–neck motor system
with increased autonomic reactivity to the test. Premature termination and autonomic
involvement without EMG signs of muscle fatigue may indicate central mechanisms.
Conclusion
The correlation between ANS and whiplash injuries has been postulated until
1920s of the last century. In the following years more evidences have progres-
sively sustained Barrè, before, and Hinoki’s, after, hypothesis. Due to the com-
plexity of the cervico-cephalic connections, the role of the ANS is not yet
completely understood, but the role of central sensitization (both at the spinal
cord and the brain level) is actually a matter of fact to explain chronicization of
WADs [27].
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Whiplash-Associated
Temporomandibular Disorders (TMDs) 12
E. Brunetta
12.1 Introduction
Rear-end impacts account for more than one-third of vehicle accidents, and nearly
40 % of these accidents produce whiplash injuries. Whiplash injury to the neck has
often been considered a significant risk factor for the development of temporoman-
dibular disorders (TMDs) [1–4].
The state in which the stomatognathic musculoskeletal system is hyperfunc-
tional, tender and exhausted is known as temporomandibular disorders (TMDs).
TMDs can generate referred craniofacial symptomatology (where origin differed
from its real location) that take influence in cervical and cranial diffuse discomfort.
TMDs consist of musculoskeletal disorders, characterized by pain in the temporo-
mandibular joint (TMJ) and/or mastication muscles, involving a wide range of cra-
niofacial conditions with multiple origins that produces a large variety of
nonobjective signs and symptoms. These could be primary, referred or combined
from cervical muscles and associated cranial structures. The most frequent symp-
tom is pain, usually localized in the muscles of mastication, the preauricular region
and the temporomandibular joint (TMJ). Patients often complain of jaw ache, ear-
ache, headache and facial pain. In addition to pain, patients with these disorders
frequently have limited or asymmetric jaw movement and joint sounds that are
described as clicking or crepitus. The pathogenesis of TMDs remains unclear, and
numerous factors have been implicated even when temporomandibular symptoms
develop following motor-vehicle collisions (MVCs). Also in these cases TMDs are
complex, representing a component of a symptom cluster of potentially regional
and widespread pain impacted by psychosocial factors. Oral health-care providers
must be aware of the complex relationship between temporomandibular symptoms
and whiplash for appropriate diagnosis and management, because TMDs following
E. Brunetta
Private Dentist, Conegliano (TV), Italy
e-mail: elvio.brunetta@fastwebnet.it

118 E. Brunetta
MVCs may result from both direct orofacial trauma and whiplash-associated disor-
der (WAD) without such trauma [5].
Furthermore, TMDs may not be identified at the time of first assessment, but
may develop weeks or more after the MVC. TMDs in WAD appear to occur pre-
dominantly in females and can be associated with regional or widespread pain.
TMDs following MVCs may respond poorly to independent therapy and may be
best managed using multidisciplinary approaches [6].
According to Salè and Isberg [7, 8] the incidence of new symptoms of TMJ pain,
dysfunction or both, between the inceptive examination and follow-up, was five
times higher in WAD subjects (34 %) than in control subjects (7 %) and 20 % of all
subjects reported that temporomandibular joint (TMJ) symptoms were their main
complaint. Visscher et al. [9] showed that, irrespective of the classification system
used, the chronic whiplash-associated disorder pain group more often suffered from
temporomandibular disorder pain (0.001 < P < 0.028) and widespread pain
(0.001 < P < 0.003) than the no neck pain group. Moreover, patients with whiplash-
associated disorder showed more psychologic distress (0.000 < P < 0.044) than oth-
ers. The higher prevalence of widespread pain and psychologic distress in patients
with chronic whiplash-associated disorder suggests that the higher prevalence of
temporomandibular disorder pain in these patients is part of a more widespread
chronic pain disorder. There appears to be a risk of delayed onset of TMDs follow-
ing an MVC. TMDs are reported as the primary complaint only by 5 % of the
patients at the first visit and by 19 % at 1-year follow-up, with painful jaw clicking
and/or locking, and they are higher in females than males.
The potential delay in onset of TMDs following an MVC raises concerns about
diagnosis, prognosis, management and medico-legal issues.
12.2 Embryology
TMJ development and other neighbouring structures in humans (such as pharynx,

Eustachian tube and tympanic cavity) is complex and continues to be investigated.
The mandible is formed from the ventral part of Meckel’s cartilage, which is the
first branchial arch. The ossicles (malleus, incus and partially the stapes) are formed
from the dorsal part of Meckel’s cartilage and Reichert’s cartilage (second branchial
arch). The malleus has a double origin in these ossicles; the anterior process origi-
nates from mesenchymal cells (os goniale), through intramembranous ossification,
and the rest form from Meckel’s cartilage, through endochondral ossification. The
malleus is related to the TMJ (condylar and temporal blastemas) by fibrous connec-
tions (lateral pterygoid muscle) passing through the petrotympanic fissure, named
the discomalleolar ligament. These lateral pterygoid muscular fibrous connections
then form the interarticular disc in Meckel’s cartilage by mechanical stimulation of
this muscle. The medial pterygoid muscle and the tensor tympani muscle develop
from the temporal blastema. These structures (along with the tensor veli palatini)
are innervated by the trigeminal mandibular branch (V3), in turn innervating the
masticatory muscles coming from the first branchial arch mesoderm.
12 Whiplash-Associated Temporomandibular Disorders (TMDs) 119
12.3 Anatomy
The temporomandibular joint (TMJ) consists of the glenoid cavity of the temporal
bone, mandibular condyle, muscles and ligaments [10]. Between the two structures
meniscus is interposed, a fibrocartilage disc connected to the joint capsule in front
of the tendon of the lateral pterygoid muscle. The rear of the glenoid cavity, or tem-
poral fossa, is very thin, and the rear tissue of the disc is sensitive to compression,
as well as light traumas with great inflammatory reactivity. The upper side (tem-
poromandibular meniscus) is used for the transfer of the jaw, and the lower side
(meniscus-condyle) is for the rotation (first 2 cm of the opening of the mouth) [11].
TMJ moves by the masticatory muscles and the supra- and infrahyoid muscles.
It is the only joint that is flat at birth and takes its shape with the masticatory func-
tion. It does this by determining its normal relationship with the temporal bone at
6 years of age, which is when the eruption of the permanent first molars determine
the vertical dimension of dental occlusion.
The innervation consists primarily of the trigeminal nerve (V cranial pair) with
three components: ophthalmic, maxillary and mandibular. Aside from the close
connections with the other cranial nerves, anatomically, their motor nuclei intersect
the brainstem reticular formation close to the basal ganglia, especially the locus
coeruleus (noradrenergic nucleus).
Furthermore, the important correlation with the innervation at the level of the cervi-
cal vertebrae has been demonstrated (see vestibule-vertebral functional unit chapter).
12.4 Biomechanics of Whiplash-Associated TMDs
Several studies have investigated concomitant functional connections between

TMDs and cervical spine disorders. The functionality of cervical and masticatory
systems is complemented synergistically but pathologically too in a concomitant
way. It has been reported [12, 13] that 45 % of TMD patients have headaches and
54 % have neck-shoulder pain confirming TMDs as a part of a more complex and
widespread painful syndrome.
Lesions present in the classic whiplash at low speed are not normally seen
through diagnostic imaging because the forces acting on the TMJ are most often
offset by the strength of the assembly-muscle ligaments of the joint, added to the
fact that the jaw weights little and has a little inertia.
WA TMD pathogenesis is still controversial. In the rear-end impact the inertia of
the mandible caused it to move posteriorly slower than the head, and this resulted in
downward and forward displacements of the disc-condyle complex relative to the
cranial base. Consequently, a rapid and big mouth opening occurs. In contrast, dur-
ing the frontal impact, the mouth hardly opened, because the superior maxilla
pushed the mandible to move together. There was no differential movement between
bony components of the joint, and therefore the soft tissues of the joint were not
subjected to high loads. Neither a rear-end impact at low velocity nor a frontal
impact would produce damage to the soft tissues of the joint.
120 E. Brunetta
In whiplash hyperextension phase of the neck, the jaw is pushed forward and
down with disc displacement in the same direction, stretching the joint capsule
with stabilizing contracture of the flexor muscles of the neck and of the supra-
and infrahyoid muscles. At the time of the hyperflexion of the neck, the jaw is
pushed upward in the posterior glenoid cavity with compression of the rear tissue
of the disc and anterior medial displacement of the disc with contracture of the
extensor muscles of the neck and jaw muscles. In this way, TMDs could be
mainly due to traumatic retrusion of the condyle either directly, since the more
sensitive anatomical part to compression is the posterior top of the glenoid cav-
ity, as already mentioned, or indirectly, through the defensive muscle spasms,
which tend to bring the jaw in retrusion, exacerbating the compression of the rear
tissue of the disc.
Recent studies have determined that about one in three people who have suffered
a whiplash injury develop TMD, even after a long time after the accident, with ten-
derness, abnormal joint kinematics, disturbances of jaw-head-neck coordination,
possible dizziness and difficulty chewing, which happens to be the highest percent-
age in women, probably because of a weaker anatomical structure [13].
Hernandez et al. [4] investigated mandibular kinematics in low-impact rear-
end impacts in 30 healthy adults. Subjects underwent three impacts (4.5 ms−2
expected, 10.0 ms−2) unexpected and 10.0 ms−2 expected). Onset time and peak
magnitude of angular head acceleration, angular mandibular acceleration and
angular mandibular displacement were measured. Significant mandibular open-
ing acceleration was not identified with rearward head rotation. The peak magni-
tude of mandibular closing angular acceleration approximately doubled with
increased impact magnitude. No differences in peak angular mandibular accel-
eration regarding expectation were identified. Gender differences were detected
in the fast unexpected impact. The peak time for the angular mandibular accel-
eration (mandibular closure) was approximately 84–120 ms later than peak rear-
ward angular head acceleration for all impacts. Onset and peak times for angular
mandibular acceleration (mandibular closure) were similar to the onset and peak
times for forward head acceleration. There was also a positive correlation
between the magnitude of the forward angular acceleration of the head and angu-
lar acceleration of the mandible for the slow (0.65, P = 0.015) and fast expected
(0.844, P = 0.001) impacts. The average angular mandibular angular displace-
ment (mandibular closure) was approximately 6°. The pure hyperextension
hypothesis regarding mechanism of TMJ injury in low-impact rear-end collisions
thus cannot be supported. Besides localized trauma to structural elements of the
stomatognathic system (peripherally mediated and maintained pain), regional
and widespread symptoms, may be due to dysfunction or dysregulation of central
pain modulating systems and regional or widespread pain input, involving neu-
ropsychological and cognitive changes (centrally mediated and maintained pain).
Altered nociceptive input and central processing in WAD patients has also been
reported in experimental pain studies.
We can conclude that the main aspect to be taken into account regarding WA
TMDs in a specific patient is the threshold of “excitability” of the system jaw-cra-
nium-neck, trigeminal controlled, as this buffer system is balanced and effective, for
Fig. 12.1 Relative displacement of the condylus with respect to the skull (glenoid) in the hyper-
extension and hyperflexion phases of whiplash
the same energy absorbed, the greater the injury-dysfunction will be minor. The
following sequence can be considered (Fig. 12.1):
1. Stretching and compression of the capsule-ligament-muscle complex of TMJ
with or without meniscal dislocation, but with the reduction of the meniscus
itself. Joint pain, myalgia, inefficient chewing, noises when opening and/or clos-
ing the mouth, sense of asymmetry in the chewing movements.
2. As above, but with dislocation and without reduction, the meniscus is blocked in
the rear part, the painful symptom is higher and the mandible kinematic is
altered, the dynamic asymmetry is evident, and the axiography reveals aspects,
possible joint locking.
3. In regard to the above, it could add micro- or macro-ligamentous injuries to the rear
tissue of the disc with possible inflammation and anatomical alteration of the joint.
12.5 TMJ and Posture
Eating requires mouth opening, biting, chewing and swallowing and should be per-
formed without dysfunction or pain. Previous studies have shown that jaw opening-
closing movements are the result of coordinated activation of both jaw and neck
122 E. Brunetta
muscles, with simultaneous movements in the temporomandibular, atlanto-occipital

and cervical spine joints. Consequently, it can be assumed that pain or dysfunction
in any of the three joint systems involved could impair jaw activities. In fact, recent
findings support this hypothesis by showing an association between neck injury and
reduced amplitudes, speed and coordination of integrated jaw-neck movements.
The jaw is connected to the skull, which is connected to the spine and skeleton
with a well-determined spatial position and is efficient for the vertical bipedal
human being. The natural law of symmetry and orthogonality determines the neu-
rogenic information of postural receptors; the cranio-cervical-mandibular posture
obeys this rule. Upper and lower jaws must be parallel and aligned with each other
in both transverse and sagittal ways and parallel to the bipupillary line, visual axis
of human, parallel to the ground itself. We understand how a perturbation that could
alter this balance can affect postural attitude.
The indirect mechanism of whiplash agent on TMJ, which determines a defen-
sive contraction of the posterior muscles of the neck, brings the line of sight upward
with a consequent hyperactivity of the muscles supra- and infrahyoid that, in order
to restore such a line, brings the mandible in retrusion triggering a possible opposed
mechanism starting from the TMJ.
The mandibular malpositioning, therefore, may cause an abnormal position of
the skull that will determine a response of the vestibular apparatus, which, through
the oculocephalic system, will try to restore the visual axis parallel to the ground
with possible asymmetries of the various components of the skeleton.
Any sagittal-type mandibular alteration, as long as symmetric, will be compen-
sated by the postural system in the opposite direction; there is, however, not the
possibility of compensation in lateral direction, as whiplash, by its nature, always
leads to asymmetric alterations which could lead to cross-like pathologies.
12.6 Diagnosis of Whiplash-Associated TMDs
WA TMD diagnosis presents considerable complexity reasons as follows:

1. The symptoms may be initially overwhelmed by the cervical one.
2. The dysfunction may develop months after the traumatic event.
3. The entity is sometimes very nuanced.
4. It is misunderstood, even by most insiders.
5. The patient may be unable to place a temporal connection with the symptoms. In
fact, Salè et al. [7] demonstrated a high frequency of inaccurate recall of TMJ
pain and dysfunction 1 year after whiplash trauma implies that clinicians and
researchers should interpret with caution the results of previous studies that
relied on retrospective data regarding whiplash-induced TMJ pain and
dysfunction.
6. Pre-existing dysfunction cannot accurately determine the cause and effect of the
trauma.
7. And, most importantly, it is very difficult to have a control group before the
event. In reality, the percentage that a patient of a dental practice, followed at a
gnathological level, suffers a whiplash injury and is reviewed by the same doctor
is very low.
To determine whether a patient who has been in a collision has a TMD, an appro-
priate history and examination of the head and neck should be undertaken, supple-
mented by diagnostic imaging, if necessary (e.g. pantomograph for screening bony
abnormalities, cone beam computed tomography scanning for more detailed bony
assessment, magnetic resonance imaging for soft tissue abnormalities). The history
should include questions related to pain in the TMJ and masticatory muscle areas
(and other areas of the head as well as the neck), TMJ sounds (e.g. clicking, crepi-
tus) and catching or locking of the jaws with opening or closing.
Various TMD classification schemes are available to allow specific diagnoses
based on the history and examination findings, but it would be desirable that every
dentist at least compose a detailed history of any TMD to create a database for moni-
toring and that examination is performed according to criteria indicated in Helkimo
index [14]. Generally speaking, it includes extraoral and intraoral palpation of mas-
ticatory muscles, evaluation of TMJ’s symmetry; investigation of tenderness/pain,
clicking or crepitus of TMJs during movements of the jaw; observation of any devia-
tion of the mandible on opening or closing; and range of mandibular movements.
Furthermore, cranial nerve function and the neck should be evaluated, including
ranges of motion and sites of tenderness in the cervical musculature, according to the
Manual Medicine procedure as described into the dedicated chapter.
Finally, on the basis of literature and personal experience, we propose to our
patients a simplified questionnaire: Whiplash Impact on TMJ Questionnaire (WITQ)
(Table 12.1).
Table 12.1 Whiplash Impact on TMJ Questionnaire (WITQ)

After your accident:
1. Have you ever had a pain in your jaw? Yes ( ) No ( )
2. Have you ever had difficulty chewing? Yes ( ) No ( )
3. Has your sleep always been normal? Yes ( ) No ( )
4. In the morning, have you ever had difficulty opening your mouth? Yes ( ) No ( )
5. Have you ever had dizziness or feelings of instability standing? Yes ( ) No ( )
It was tested on 20 patients already compensated by insurance in order to not be influ-

enced by possible additional complaints. Patients were heterogeneous regarding age, sex,
social position and the characteristics of the accident, but all of them had problems related
to TMD (joint pain, difficulty chewing, unsatisfactory sleep, any equilibrium distur-
bances) followed at least 6 months after the collision. Seven patients (4 females and
3 males) answered affirmatively to all questions, four (2 females, 2 males) referred only
TMJ pain, seven answered negatively, two patients did not answer. Despite the small
sample, this simplified method agrees with the studies in the literature that lead to about
30 %, the percentage of referred TMDs after a MCV with whiplash.
124 E. Brunetta
12.7 Therapy
Multidisciplinary dental and medical management is necessary in many patients,

and TMDs in these situations should not be interpreted as separate, independent
conditions. Dentists should provide appropriate conservative, reversible forms of
TMD management as part of a multidisciplinary team approach in order to eliminate
or mitigate the pain as much as possible and restore a normal mandibular kinematic.
Apart from the use of pain medication and/or anti-inflammatory, benzodiaze-
pines at low dosage for few days before sleeping is necessary, as this disease is more
active especially at the end of the night, disturbing the normal rest.
Generally, we suggest that patients follow a programme of physical therapy,
occupational therapy and pain management. At the start of their stay, they have to
be examined both by a physician specialized in rehabilitation medicine and a dentist
to perform a complete functional examination, both of the stomatognathic system,
shoulder girdle and spine. This kind of programme is useful especially to increase
maximum active mouth-opening capacity, but some authors [15] showed that thera-
peutic jaw exercises, in addition to the regular whiplash rehabilitation programme,
did not reduce symptoms and signs of WA TMDs.
For this reason we combine physical therapy with low-level laser therapy (LLLT)
directed on painful TMJ, main stomatognathic, cervico-dorsal trigger and tender
points. This combination, from our experience, yielded the best results especially in
cases without dislocation of the disc.
Other valid therapy is intraoral plates that are irreplaceable in cases with disloca-
tion of the disc or joint locks.
The use of such devices must be well calibrated, especially in thickness, because
when altering the vertical dimension (dimensional relationship between the dental
arches), it is necessary to be sure that the system can tolerate the “new” jaw posture.
It is also essential to check the correctness of the device with postural tests and pos-
sibly by the mean of stabilometry (see Chapter 17 on “Static posturography and
whiplash” by P.L. Ghilardi, A. Casani, B. Fattori, R. Kohen-Raz and Dario C. Alpini).
12.8 Prognosis
Approximately 15–40 % of patients with acute WAD develop chronic symptoms

[2]. Chronic WAD represents a physical, medical, economic and psychosocial prob-
lem. Severe neck pain, self-reporting of poor general health and stress in WA TMD
patients are similar to that of nontrauma TMD patients, although the posttraumatic
patients frequently require constant analgesic assumption, suggesting persistence of
pain. In contrast, De Boever et al. [16] comparing two groups of TMD patients—
one without a history of trauma to the head and neck (302 patients) and the other
with a history of trauma that was linked to the onset of symptoms (98 patients)—
showed that the trauma group’s symptoms were more pronounced initially, but both
groups responded equally well to conservative treatment after 1 year. Despite these
findings, a minority of individuals develop a chronic condition that may reflect the
more complex nature of regional and widespread pain, which may be the result of
central hypersensitivity mechanisms or possible mild traumatic brain injury.
Romanelli et al. [17] confirmed that post-MVC TMD patients do not respond to
management and require more treatment compared to nontrauma cases. Other stud-
ies have demonstrated similar findings.
TMDs that develop post-MVC have a less favourable prognosis and affect qual-
ity of life. Anyway, most patients who develop TMDs following an MVC often
improve with time or with standard therapy: active coping strategies (activity and
exercise) is, in our experience, one of the most important aspects for recovery, while
pessimism regarding return to usual activities may affect positive outcome.
References
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3. Grönqvist J, Häggman-Henrikson B, Eriksson PO (2008) Impaired jaw function and eating
difficulties in whiplash-associated disorders. Swed Dent J 32(4):171–177
4. Hernández IA, Fyfe KR, Heo G, Major PW (2006) Mandibular kinematics associated with
simulated low-velocity rear-end impacts. J Oral Rehabil 33(8):566–575
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associated disorders. Arch Oral Biol 52(4):404–408. Epub 2007 Feb 1
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following motor vehicle collisions: part 2. Temporomandibular disorders. J Can Dent Assoc
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pain and dysfunction after experiencing whiplash trauma: a prospective study. J Am Dent
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Whiplash and Sport
13
M. Albano, D.C. Alpini, and G.V. Carbone
13.1 Introduction
Although sports-related injuries to the head and neck are much less common than
injuries to the extremities, an estimated 70 % of mortality and 20 % of permanent
disability result from injuries to the head and neck [1].
Whiplash is a term that refers to neck injuries that are incurred after the neck is
forcibly bent forward, backward or both. Whiplash is a common injury associated
with contact sports such as football, rugby and hockey. Symptoms of whiplash
include neck pain and stiffness, pain in the back, arms and shoulders, dizziness,
problems with concentration, blurred vision, ringing in the ears and irritability and
patient needs an accurate diagnosis and appropriate treatment.
Head and neck injuries often occur simultaneously, and whiplash is often asso-
ciated to concussion. Concussion is defined as a traumatically induced transient
disturbance of brain function and involves a complex pathophysiological process.
Concussion is a subset of mild traumatic brain injury (MTBI) which is generally
self-limited and at the less-severe end of the brain injury spectrum [2]. Head and
neck common injuries are frequent in American football, hockey and rugby that
have the highest incidence of concussion, while soccer has the lowest. Male box-
ers and female taekwondo participants have the highest frequency of concussion
M. Albano (*)
Sport Physiatrist “Galileo 18” Physiotherapy Centre, Juventus Football Club Medical Team,
C.so Galileo Ferarris 18, Turin, Italy
e-mail: michele.albano4@virgilio.it
D.C. Alpini
Milan, Italy
e-mail: dario.alpini@fastwebnet.it
G.V. Carbone
“Istituto Clinico Città Studi” City Hospital, Milano Hockey Medical Team,
via Jommelli 17, Milan, Italy

128 M. Albano et al.
at the recreational level [3], and evidence indicates that female athletes may be at
greater risk for concussion than their male counterparts. There also is some evi-
dence that gender differences exist in outcomes of traumatic brain injury and
concussions [4, 5].
Pure neck injuries in sports are less common, typically debilitating, and quite
predictable in retrospect by mechanism of injury as to one of four natures – sprains/
strains, fractures, brachial plexus pinches/stretches and spinal cord injury. Of these,
the spinal cord injury, whether a concussion or contusion or physical disruption, is
obviously the most severe (so-called Quebec Task Force WAD grade IV) and also,
ironically, the best tracked because of its definition and notoriety when it is experi-
enced [6–8].
The medical problem of neck injuries in sport is two-folded: diagnosis and treat-
ment of acute lesion and adequate programming of athlete returning to sport prac-
tice. While most people can return to everyday activities a few days after sustaining
a whiplash injury, athletes, in fact, need to achieve a full recovery before getting
back on the field. Even if they feel ready, it’s important to be completely free of
whiplash symptoms and have medical clearance before returning to sports.
13.2 Neck Injuries in Sport Practice
Neck injury usually is secondary to high-velocity collisions between players, caus-

ing acceleration or deceleration of the head on the neck. Acceleration usually causes
a whiplash type of extension force on the neck, while deceleration usually results in
flexion forces. Serious injuries with neurological sequelae remain infrequent and
most of these injuries are self-limited.
Regarding sport epidemiology, Tsoumpos et al. [9] recorded over 150 injuries
between the years of 2008 and 2011, especially in contact sports, including indoor
soccer, basketball, and wrestling but also in several noncontact sports, such as
diving.
Whiplash spine injuries are estimated to occur in high percentage of indoor soc-
cer players, and most commonly on defensive players.
According to the authors, there is no practical difference with healthy control
group normalised with regard to sex, age, socioeconomic status and marital status
after 6 months from initial trauma. They concluded that even if there is a significant
risk of whiplash-type injuries in sports, serious injuries with neurological sequelae
and chronic whiplash-associated disorders (QTF WAD grades III and IV) remain
very infrequent.
Anyway, cervical spine injuries remain a serious concern in some games like
American football, in which they have been estimated to occur in 10–15 % [10] of
football players, most commonly in linemen, defensive ends and linebackers.
Also in ice hockey players, cervical injuries are frequently observed even if
the overwhelming majority of such injuries are self-limited, and full recovery
13 Whiplash and Sport 129
can be expected. However, the presenting symptoms of serious cervical spine

injuries may closely resemble those of minor injuries. The orthopaedic surgeon
frequently must make a judgment, on the field or later in the office, about the
advisability of returning the athlete to the game. These decisions can have an
enormous impact on the player, his team and his family. Most severe cervical
spine injuries share the common mechanism of application of an axial load to the
straightened spine. Advances in specific sport techniques, rules of the game and
medical care of the athlete have been made throughout the past few decades to
minimise the risk of cervical injury and improve the management of injuries that
do occur.
Injuries have a wide spectrum of severity. The relatively common ‘stinge’ is a
neuropraxia of a cervical nerve root(s) or brachial plexus and represents a reversible
peripheral nerve injury. Less common and more serious an injury, cervical cord
neuropraxia is the clinical manifestation of neuropraxia of the cervical spinal cord
due to hyperextension, hyperflexion or axial loading.
Recent data [11] on American football suggest that approximately 0.2 per
100,000 participants at the high school level and 2 per 100,000 participants at the
collegiate level are diagnosed with cervical cord neuropraxia. Characterised by
temporary pain, paraesthesias and/or motor weakness in more than one extremity,
there is a rapid and complete resolution of symptoms and a normal physical exami-
nation within 10 min to 48 h after the initial injury.
Stenosis of the spinal canal, whether congenital or acquired, is thought to predis-
pose the athlete to cervical cord neuropraxia. Although quite rare, catastrophic neu-
rological injury is a devastating entity referring to permanent neurological injury or
death. The mechanism is most often a forced hyperflexion injury, as occurs when
‘spear tackling’.
The mean incidence of catastrophic neurological injury over the past 30 years
has been approximately 0.5 per 100,000 participants at high school level and 1.5 per
100,000 at the collegiate level. This incidence has decreased significantly when
compared with the incidence in the early 1970s. This decrease in the incidence of
catastrophic injury is felt to be the result of changes in the rules in the mid-1970s
that prohibited the use of the head as the initial contact point when blocking and
tackling [12].
In professional rugby union players, incidence, severity, nature, and causes of
cervical, thoracic, and lumbar spine injuries sustained during competition and train-
ing have been studied by Fuller et al. [13]. They identified as risk factors player age,
body mass, stature, playing position, use of headgear and activity and period of
season. In their study the incidences of spinal injuries were 11 per 1,000 player
match-hours and 0.37 per 1,000 player training hours. No player sustained a cata-
strophic spinal injury, but three players sustained career-ending injuries. Overall,
players were more likely to sustain a cervical injury during matches and a lumbar
injury during training. Forwards were significantly more likely to sustain a spinal
injury than backs during both matches and training. During matches, injuries to the
cervical and lumbar spine were more severe (calculated as days necessary to sport
practice recovery) than injuries to the thoracic spine; during training, injuries to the
lumbar spine were more severe than cerebral injuries.
Similar differences regarding injuries occurred during matches with respect to
training have been observed also in professional soccer players. Nilson et al. [14],
in a recent investigation, recorded a total of 136 head and neck injuries, that is to
say 2.2 % of all injuries. The head and neck injury rate was 0.17 (0.06 concus-
sions) per 1,000 h. There was a 20-fold higher rate of head and neck injury during
match play compared with training and a 78-fold higher rate of concussions.
Mean layoff for concussion was 10.5 days, but 27 % of the concussed players
returned to play within 5 days. Defender was the playing position most at risk.
Authors highlight that more than one-quarter of the concussed players returned to
play before what is recommended in the consensus statements by the major sports
governing bodies.
Kochar et al. investigated the risk of cervical injuries in mixed martial arts [15].
The kinematics of the athletic acts of these sports, from the point of impact, bears
a considerable resemblance to the kinematics of a rear-end motor vehicle collision.
With respect to car collisions, it has been shown that the biomechanics, kinetics and
kinematics all contribute towards the outcome. It can be seen that the impact with
the opponent on the ground can be directly correlated with the moment of impact in
a rear-end collision. If one compares the force imparted on the driver from the seat
with the reaction force of the ground on the opponent, one can see that they act at
similar sites and in similar directions. There is also similar posterior translation of
the head after impact in some martial arts manoeuvres (such as goshi and souplesse)
and the car impact models. The action of the force causing pathological neck motion
is of similar magnitude in the two scenarios (car and martial arts), and the gross
pattern of motion seems to be comparable, including the mechanical obstruction
from hyperextension of the cervical region by the floor and the car seat headrest,
respectively.
13.3 The Role of Sideline Physician in the Management

of Head and Neck Injuries
Head and cervical spine sports-related injuries are intimately associated. The on-
field evaluation and management of the athlete with these injuries is of paramount
importance to stabilise the athlete and prevent further injury.
The incidence of catastrophic cervical spine injury in sports is low compared
with other sport injuries. However, cervical spine injuries necessitate delicate and
precise management, often involving the combined efforts of a variety of health
care providers. The outcome of a catastrophic cervical spine injury depends on the
efficiency of this management process and timeliness of transfer to a controlled
environment for diagnosis and treatment.
One of the most challenging roles of the team physician involves the intervention
and decision-making processes regarding cervical spine injuries in contact sports.
The team physician must be well versed in the prevention, evaluation, stabilisation
and treatment of spine injuries. A high index of suspicion and an understanding of
cervical alignment and architecture, as well as comprehension of the mechanics
exerted during a sporting event, are imperative to diagnosing cervical injuries.
Sideline physicians must be attentive and prepared with an organised approach
to detect and manage these injuries [16]. Evaluation of patients with suspected cer-
vical spine injury includes a complete neurological examination while on the field
or the sidelines. Immobilisation on a hard board may also be necessary. The deci-
sion to obtain radiographs can be made on the basis of the history and physical
examination.
The goal in assessing neck injuries is to detect spinal cord injury and the poten-
tial for such injury resulting from instability of the cervical spine.
Cervical spine instability and the accompanying potential for neurological loss
may be commonly underdiagnosed. The evaluation of neck injuries requires a regi-
mented examination and a defined management protocol. A stepwise evaluation
(Table 13.1), including a Spurling test that is to say a foraminal compression test,
has to be used to evaluate cervical nerve root injury. In Spurling test, the examiner
actively compresses the right and left foramina. Cervical radiculopathy is indicated
if this position elicits radicular symptoms in the upper limb. Each step [17] in this
examination presents a progressively greater risk to the spinal cord; therefore, if
any part of the examination is abnormal, instability is presumed and testing is
stopped. Furthermore, if an abnormality is found at any point of the examina-
tion, the neck should be immobilised and the patient prepared for transport to an
emergency department. Any focal neurological symptom suggests a potential cen-
tral nervous system injury. In particular, bilateral symptoms must be considered
carefully [18].
Table 13.1 Combined Evaluation of Head and Neck Injuries (Whiteside [17])
1. Note the exact time of injury. Management decisions are based on duration of
symptoms
2. Assess loss of consciousness. Management of unresponsive athletes should follow
the ABCs of trauma care (i.e. check airway, breathing, and circulation)
3. Assess peripheral strength and sensation without moving the athlete’s head or neck
4. Palpate the neck for asymmetric spasm or tenderness at the spine
5. Assess isometric neck strength without moving the athlete’s head or neck
6. Assess active range of motion at the neck
7. Perform axial compression and Spurling test. If negative, athlete may be moved
8. Assess recent memory and postural instability
9. Inquire about symptoms such as headache, nausea, dizziness or blurred vision
This neck evaluation guideline cannot be used with unconscious athletes, and the
detection of an unstable fracture is impossible. Instead, instability must be assumed,
and care must be taken to avoid manipulation of the neck. In the absence of immedi-
ate danger, an unconscious injured athlete should remain at the site of the injury
until the spine is fully immobilised. Three or four trained persons are required to
safely ‘log roll’ the athlete into a supine position on a backboard. This procedure
may require leaving the patient at the site until emergency medical personnel arrive.
The physician should remind others involved in assisting the player that preventing
further injury is the priority; the athlete should not be rushed from the field for the
sake of continuing play [19].
Sideline physicians must protect the spinal cord from injury whenever instability
is a consideration. A cervical collar alone never should be considered adequate pro-
tection for the spinal cord. Instead, full immobilisation on a backboard is required
to stabilise the neck. When immobilising the neck, physicians should avoid move-
ment and maintain proper alignment of the cervical vertebrae. This usually can be
done with the helmet and other protective gear (e.g. shoulder pads) in place, and
such equipment should not be removed. Studies using American football equipment
on cadavers showed that removing the helmet and shoulder pads results in excessive
movement of the cervical spine.
Symptoms of concussion are neurological in nature, occur immediately after a
trauma and are transient. Concussion is common in sports; by conservative esti-
mates, there are more than 300,000 sports-related concussions in the United States
each year [20]. However, studies of relatively mild brain injuries, such as those typi-
cally sustained in sports, are limited.
Graded symptom checklists provide an objective tool for assessing a variety of
symptoms related to concussions, while also tracking the severity of those symp-
toms over serial evaluations. Standardised assessment tools provide a helpful struc-
ture for the evaluation of concussion:
1. Assessment for loss of consciousness (LoC)
2. Inquiring about symptoms commonly associated with concussion
3. Evaluating recently acquired memory
4. Evaluating postural stability
Any athlete suspected of having a concussion should be stopped from playing
and assessed by a licenced healthcare provider trained in the evaluation and man-
agement of concussions. Team physicians should restrict from play any athlete with
persistent symptoms of concussion because these symptoms place them at risk of
reinjury if they return prematurely. Recognition and initial assessment of a concus-
sion should be guided by a symptoms checklist, cognitive evaluation (including
orientation, past and immediate memory, new learning and concentration), balance
tests and further neurological physical examination.
Concussion is defined by transient symptoms, and until those symptoms resolve,
other diagnoses must be considered. Athletes with memory loss, imbalance or
symptoms reported 15 min after the injury should be restricted from play for the rest
of the day. Athletes with neurological symptoms persisting longer than 30 min,
particularly those with prolonged LoC or any focal neurological sign, should be
monitored closely and may require transport to an emergency department. Finally,
athletes with seizures, persistent vomiting or suspected skull fracture should be
urgently evaluated in an emergency department.
Balance disturbance is a specific indicator of a concussion, but not very sensitive.
Balance testing on the sideline may be substantially different than baseline tests
because of differences in shoe/cleat-type or surface, use of ankle tape or braces or
the presence of other lower extremity injury.
Imaging is reserved for athletes where intracerebral bleeding is suspected.
Athletes suspected or diagnosed with a concussion should be monitored for deterio-
rating physical or mental status with neuropsychological (NP) tests, as an objective
measure of brain-behaviour relationships, more sensitive for subtle cognitive
impairment than clinical exam. Anyway, it is unknown if use of NP testing in the
management of sports concussion helps prevent recurrent concussion, catastrophic
injury or long-term complications [2].
13.4 Recovering from Head and Neck Trauma
Treatment depends on the severity of diagnosed injury and can range from an indi-
vidualised cervical spine rehabilitation programme for a ‘stinger’ (QTF WAD I
grade) to cervical spine decompression and fusion for more serious bony or liga-
mentous injury (QTF WAD IV grade). Still under constant debate is the decision to
return to play for the athlete.
After resting for a day or two, patients recovering from mild to moderate whip-
lash should resume normal physical activity so that they can work their muscles and
maintain flexibility in their soft tissue. Patients suffering from more severe whiplash
may require a longer period of rest and should resume activity based on the advice
of a doctor. If whiplash patients remain inactive for too long, pain will actually
become more severe and difficult to treat. This does not mean that whiplash suffer-
ers should immediately return to contact sports. While a return to daily activity is
recommended, anyone recovering from whiplash should avoid heavy lifting, severe
neck strain, intensive stretching and risky behaviour including contact sports until
they have fully recovered.
A history of concussion is associated with a higher risk of sustaining another
concussion. A greater number, severity and duration of symptoms after a con-
cussion are predictors of a prolonged recovery. In sports with similar playing
rules, the reported incidence of concussion is higher in female athletes than in
male athletes. Certain sports, positions and individual playing styles have a
greater risk of concussion. Youth athletes may have a more prolonged recovery
and are more susceptible to a concussion accompanied by a catastrophic injury.
Preinjury mood disorders, learning disorders, attention deficit disorders (ADD/
ADHD) and migraine headaches complicate the diagnosis and management of a
concussion.
13.5 Criteria for Returning to Practice (RTP)
Serious injuries with neurological sequelae remain infrequent, and most of cervical
injuries are self-limited. Injuries occur in all levels of play from the high school to
the professional level. The decision of return to play following cervical spine inju-
ries can be one of the most challenging with a wide variation in opinion as far as
management.
In general, the literature [21–24] shows agreement for the basic necessities for
return to collision sports to include normal strength, painless range of motion, a
stable vertebral column and adequate space for the neurological elements. In addi-
tion, return to play in an unsafe environment is contraindicated.
Playing with defective equipment or with improper technique has been associ-
ated with catastrophic injuries and should be avoided. This particularly includes
spear tackling, diving in unknown or shallow water, diving while intoxicated, check-
ing from behind in hockey or using a trampoline without spotting equipment.
However, there is a lack of consensus on returning to play with the following:
stenosis, spear tackler’s spine, loss of normal lordosis or range of motion, surgically
corrected instability, ligamentous instability, transient quadriparesis, healed disc
herniation and congenital fusion.
Since contact sports can exacerbate a whiplash injury, patients should not return
to sports like football, wrestling or hockey until given a clean bill of health by their
doctors. Some doctors may recommend a return to practice or noncontact drills
while recovery is still in progress, but a full-contact game is not advisable until pain
and tenderness in the neck area has subsided completely.
Figure 13.1 is referred to two hockey players. They are homozygote twins, play-
ing with the same role in the same hockey team. Head-to-neck stability has been
calculated as mean head and trunk velocities while standing with eyes open or
closed on firm or foam surface. Mean head and trunk velocities have been calcu-
lated by means of two accelerometers (Delos device, Turin, Italy) posed on the head
and the sternum (for details, see chapter 19 and reference [25]). Both athletes were
studied 12 h after the match. Player 2 reported a whiplash trauma during a strong
contact. Posturography clearly shows how the head is unstable with respect to the
trunk even simply standing.
Patients should experience a full range of motion in their necks, shoulders and
arms, maintain proper pre-injury posture and pass a neurological assessment before
engaging in any contact sport. If a player returns to sport prematurely, the risk of
further injury to the neck is increased significantly. If the athlete experiences any
long-term effects of whiplash, such as headache, chronic pain or problems with
range of motion, he/she has to cease his/her participation in contact sports and con-
sult a doctor as soon as possible.
The non-elite athlete may not have the same resources available as the elite ath-
lete (such as the presence of trained medical staff during practise and competition,
a concussion programme as part of sideline preparedness, the benefit of neuropsy-
chological or postural testing, as well as consultants with expertise in concussion
readily available) and as a result will generally be managed more conservatively.
Player n. 1 Player n. 2
29 30
Vel head Vel head
28 25
Vel trunk Vel trunk
27
20
26
25 15
24
10
23
5
22
21 0
EO EC EO foam EC foam EO EC EO foam EC foam
Fig. 13.1 Posturographic recording of head-to-trunk stability in stance after a hockey match.
Mean head and trunk velocities have been calculated by means of two accelerometers (Delos
device, Turin, Italy) posed on the head and the sternum. Players were required standing with eyes
open or closed on firm or foam surfaces. Even both players show head velocity higher than trunk
velocity when standing on firm surface with eyes open, only player 2 shows clear head instability
in all four tests. Players are homozygote twins, playing with the same role in the same hockey
team. Both athletes were studied 12 h after the match. Player 2 reported a whiplash trauma during
a strong contact. Posturography clearly shows how the head is unstable with respect to the trunk
even simply standing
Younger athletes often have a greater incidence of concussion with longer recovery
time frames; however, they are often managed with less expertise and with limited
resources.
Child athletes take longer to recover from concussions than adults. Concussion
symptoms may resolve before cognitive function has completely recovered.
Concussion assessment and management in children can be confounded by their
growth and development, as well as the lack of trained medical personnel involved
with youth sports. There are no child-specific assessment tools for concussion. RTP
decisions in children should be made cautiously and should be individualised. No
concussed child athlete should be allowed to RTP the same day. Physical and cogni-
tive rest is very important to allow for the resolution of concussion symptoms. Child
athletes should remain symptom free for several days before starting a medically
supervised stepwise exertion protocol. Further research is needed to elucidate the
effects of concussion in children and to determine the most appropriate RTP guide-
lines. Child-specific concussion assessment tools need to be developed to improve
concussion assessment and management in children.
13.6 Preventing Future Injury
Primary prevention of some injuries may be possible with modification and enforce-
ment of the rules and fair play. Helmets, both hard [25] (football, lacrosse and
hockey) and soft (soccer, rugby), are best suited to prevent impact injuries (fracture,
bleeding, laceration, etc.) but have not been shown to reduce the incidence and
severity of concussions [26]. There is no current evidence that mouth guards can
reduce the severity of or prevent concussions.
Secondary prevention may be possible by appropriate RTP management. Players
must be careful when returning to contact sports so that they don’t suffer from a
repeat injury. Athletes who have experienced whiplash should perform specific
exercises designed to strengthen their necks. A stronger neck with an expanded
circumference of at least 1 cm can protect them from future whiplash injuries. They
should also ensure to warm up properly before entering the playing field or working
out at the gym. Playing football or hockey requires investing in high-quality, prop-
erly fitted neck and shoulder pads to protect the neck.
Ice hockey and American football are violent collision sport, and neck injuries
are an unavoidable part of the game. What can be improved are the preventative
measures, the treatment techniques and some standardisation of risk factors in play-
ing after a neck injury. Prevention starts with decreasing the use of the head as an
offensive weapon in American football and with proper shoulder pads in both
sports.
Treatment begins with proper on-field evaluation and transportation techniques
and is completed by good consultation services. Proper evaluation of risk demands
requires open discussions with the patient of all factors involved. Clear advice has
to be given to players and to the team through their medical staff [27].
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Whiplash Associated Somatic Tinnitus
(WAST) 14
D.C. Alpini, A. Cesarani, and A. Hahn
14.1 Introduction
Approximately 10 % of patients who have suffered whiplash injury will develop

otological symptoms such as tinnitus, deafness and vertigo [1]. Some of these are
purely subjective symptoms. Tinnitus is a common and disturbing symptom; it is
the perception of ringing, buzzing, hissing, or other noises in the ears or head in the
absence of external sources for these sounds. These perceptions can be transient,
intermittent, occasional, or constant. “Chronic” tinnitus is present all or most of the
time during a person’s waking hours.
Tinnitus is therefore also considered an auditory phantom percept similar to
central neuropathic pain. Its pathophysiology remains unclear, but it is supposed to
result from hyperactivity and neuroplastic pathological reorganization of cortical–
subcortical auditory and nonauditory networks [2].
Chronic disabling tinnitus is due to emotional–affective involvement induced by
a pathological shift of patient attention to his/her tinnitus. Coping with tinnitus thus
requires a modification of the patient approach to one’s self-perception through the
modification of lifestyle, stressor removing and diverting pathological attention.
The aim of the tinnitus cure, generally speaking, is to reach a golden point in which
the patient is able to hear tinnitus but tinnitus is not disabling for the patient.
D.C. Alpini
A. Cesarani
A. Hahn (*)
3ENT Clinic, 3rd Medical Faculty, Charles University Prague, Prague, Czech Republic
e-mail: hahn@fnkv.cz

Whiplash associated tinnitus could be due to an auditory damage, as a conse-

quence of inner ear damage with hearing loss due to labyrinth concussion or verte-
bral artery spasm. In these cases tinnitus has to be mainly treated into the context of
inner ear damage treatment.
In some cases, tinnitus, even without any significant hearing loss, could be
related to whiplash injuries of the temporomandibular joint (TMJ) and upper cervi-
cal spine through the interaction between the somatosensory and auditory systems.
In these patients, neck and/or facial movements, movements of the upper extremi-
ties, tactile stimulation, changes in gaze, jaw opening or teeth clenching may induce
or modulate tinnitus: the so-called somatic tinnitus.
Somatic tinnitus is a subgroup of tinnitus suffers. It was described by Pulec et al.
in 1978 [3] as “cervical tinnitus”, considered as a consequence of degenerative
changes in the cervical spine that could be, at least temporarily, reduced by injection
of local anaesthetic into tender areas of the neck. This clinical entity was forgotten
until Dehmel et al. [4] introduced the somatic tinnitus syndrome (STS) in which
tinnitus is associated to a somatic disorder involving the head and neck. They pre-
sented the anatomical basis for the auditory–somatosensory interactions and showed
how auditory neurons respond to somatosensory stimulation.
Particularly, whiplash associated muscle–skeletal disorders could become a
chronic stress source that pathologically integrates with previous or whiplash-induced
auditory disturbances, causing/increasing tinnitus. More specifically, somatic tinnitus
suffers frequently present modulation of their spontaneous tinnitus through appropri-
ate stimulation of trigger points in the cervical and shoulder muscles. Somatic tinnitus
occurs when the patient feels the effect of head and neck muscle contractions, chang-
ing the intensity or quality of tinnitus, for instance, during clenching the teeth or head
rotation. In these cases, tinnitus is modulated by stimulation of the somatosensory
system as a result of muscle contractions. This is not surprising because the auditory
system is part of the most complex sensory–motor system involved in the head posi-
tion regulation, necessary to provide gravitation reference, prerequisite for a correct
orientation of the human subject in the environment. The brainstem and cerebellum
are the main sites of integration of multi-sensorial information from the inner ear,
retina and proprioceptors regarding head position, body position, gravity, visual land-
marks and movement of the jaw, the tongue and the pharynx.
Somatic tinnitus, generally, is a well-treatable condition by means of manipula-
tions, physiotherapy and physical exercises, or at least, the removal of somatic com-
ponent of patient’s tinnitus significantly decreases tinnitus annoyance and improves
quality of life.
14.2 Diagnosis of Whiplash Associated Somatic Tinnitus

(WAST)
The convergence between auditory and somatosensory inputs was shown by

Levine et al. [5]: forceful manipulations or contractions of the muscles of the jaw,
head or neck elicited the perception in 58 % of the subjects. Several studies have
14 Whiplash Associated Somatic Tinnitus (WAST) 141
demonstrated the interactions between the somatosensory and auditory systems at

the dorsal cochlear nucleus (DCN) [6], inferior colliculus and parietal association
areas. In particular, auditory and somatosensory [7, 8] (proprioceptive and tactile)
pathways converge into specialized multisensory brain areas, particularly the
right inferior frontal gyrus and both right and left insulae, that work as multisen-
sory operators for the processing of stimulus identity. In animals, it was shown
that hyperactivity in the DCN, which is a second-order auditory structure [9],
correlates with noise-induced tinnitus [10]. The DCN receives auditory input
from the VIIIth nerve and somatosensory input, directly from the ipsilateral dor-
sal column and spinal trigeminal nuclei or indirectly via the dorsal raphe and
locus coeruleus.
Diagnosis must combine investigation of auditory condition and somatic cervico-
cephalic condition. Diagnosis is threefold:
1. Identification of eventual auditory damage and main tinnitus characteristics.
2. Forceful manoeuvres of the neck and the mouth (so-called somatic tests) to iden-
tify somatic component of tinnitus: the more prevalent the somatic component,
the higher the possibilities to cure tinnitus.
3. Identification of emotional and cognitive aspects of tinnitus-induced
disturbances.
14.2.1 Identification of Eventual Auditory Damage and Main

Tinnitus Characteristics
Pure tone audiometry and tympanometry are the basic steps to identify hearing loss.
In this case it will be necessary to proceed as indicated in the specific chapter dedi-
cated to inner ear WAD. The loudness of tinnitus can be estimated by asking the
individual to adjust an external sound so as to match the loudness of the tinnitus.
One method is for the listener to first select a sound that is similar to their tinnitus.
For example, if the tinnitus is tonal, the listener might adjust the frequency of a pure
tone until it matches the pitch of their tinnitus. Then, the external tone is adjusted in
level so as to match the loudness of the tinnitus. For the scope of WAST assessment,
Feldman test [11] and loudness discomfort level test [7] are enough to investigate
auditory/somatic interaction under a therapeutic point of view.
14.2.2 Forceful Manoeuvres of the Neck and the Mouth

(So-Called Somatic Tests) to Identify Somatic Component
of Tinnitus: The More Prevalent the Somatic Component,
the Higher the Possibilities to Cure Tinnitus
Levine et al. [5] proposed to identify somatic components of tinnitus through a

series of forceful manoeuvres or pressures on some parts of the head or the neck,
during which patients has to note modification of tinnitus loudness or pitch
(Table 14.1)
Table 14.1 Somatic Testing According to Levine et al. [5]
All manoeuvres use maximal force applied by the examiner

(a) Jaw contractions
Clench teeth together
Open mouth with and without restorative pressure
Protrude jaw with and without restorative pressure
Slide jaw to the left and the right with and without restorative pressure
Retrude jaw
(b) Head and neck contractions
With the head in the neutral position, contractions were made to resist pressure applied
by the examiner to the:
Forehead
Occiput
Vertex
Left and right temple
With the head turned to the left, before, and to the right, after, resist the torsional force
on the ipsilateral zygoma
With the head turned to the right and tilted to the left, before, and vice versa, after,
resist force applied to the opposite temple (to test the sternocleidomastoid)
(c) Pressure on muscle insertions
Right and left mastoid attachment of the sternocleidomastoid
Right and left suboccipital attachment of the splenius capitis
Posterior pinna pressure
Right and left pinna attachment of the posterior auricular
Furthermore, examination protocol includes:
(d) Estimation of neck range of movement in the three directions, in degrees
(e) Palpation of the right and left trapezius, temporalis, masseter, medial pterygoid. For
each muscle bulk tender and tension are subjectively quantified ranging from 0 to 5
We have simplified the examination protocol as follows:
1. Jendrassik manoeuvre
2. Clench the teeth together – forced opening of the mouth – and protrude the jaw
with and without restorative pressure
3. With the head in the neutral position, contractions to resist pressure applied by the
examiner to the forehead and occiput
On the basis of the results of these main manoeuvres, an accurate [12] evaluation/
palpation of the TMJ and stomatognathic muscles and/or cervical and dorsal spine
according the examination criteria of Manual Medicine as described elsewhere in the
book (see Chap. 17 “Static Posturography and Whiplash” by P.L. Ghilardi, A.
Casani, B. Fattori, R. Kohen-Raz, and Dario C. Alpini) is therefore performed.
Generally speaking, Manual Medicine examination is mainly aimed to identify trig-
ger and tender points of the facial and cervico-dorsal muscles. Trigger points are
described as hyperirritable spots in the skeletal muscle that are associated with pal-
pable nodules in taut bands of muscle fibres. Trigger points are small contraction
knots and a common cause of pain. Compression of a trigger point may elicit local
tenderness, referred pain or local twitch response. It is common to induce transient
tinnitus when stimulating trigger points in the trapezius muscle. A tender point hurts
to the touch and causes some degree of pain in that area, while a trigger point may
not necessarily be painful to the touch but causes a degree of pain (or tinnitus in this
specific field of investigation) to be felt in another area. Furthermore, Manual
Medicine looks for the so-called painful minor intervertebral dysfunctions (PMID),
in these cases, paying particular attention to the cervical and dorsal spine [13].
Particular attention is also paid to temporomandibular disorders (TMDs) very
often underdiagnosed in whiplash patients (see dedicated chapter). TMDs are a group
of related disorders of the masticatory system (the masticatory musculature and the
temporomandibular joint). The most frequent symptom is pain, usually localized in
the muscles of mastication, the preauricular region and the temporomandibular joint
(TMJ). Patients often complain of jaw ache, earache, headache and facial pain. In
addition to pain, patients with these disorders frequently have limited or asymmetric
jaw movement and joint sounds that are described as clicking or crepitus.
The Jendrassik manoeuvre is useful to identify a specific activation of tinnitus,
while Manual Medicine examination procedure provides the basis of the manipula-
tive treatment. When TMDs are prevalent, manipulative and physical treatments
have to be combined with adequate stomatognathic therapy.
14.2.3 Identification of Emotional and Cognitive Aspects

of Tinnitus-Induced Disturbances
The Tinnitus Reaction Questionnaire (TRQ) [14] is useful to identify the tinnitus
stress-induced phase of a specific patient. TRQ is a self-reported scale designed to
assess perceived distress associated with tinnitus. It is composed of 26 items describ-
ing some of the potential effects of tinnitus on lifestyle, general well-being and
emotional state. Respondents are asked to rate the extent to which each of the poten-
tial effects has applied to them over the last week on a 5-point scale (0, not at all; 4,
almost all the time). Respondents are also asked to indicate how frequently tinnitus
induces some reactions such as depression, anger and confusion (from not at all to
always). The total score ranges from 0 to 104. A lower score represents slight reac-
tion to tinnitus, while higher scores indicate deeply negative reaction.
To determine individual tinnitus-specific reaction besides TRQ, the Tinnitus
Cognitive Questionnaire (TCQ) [15] was adopted. TCQ investigates patient
approach to tinnitus with 13 negative (1–13) and 13 positive (14–26) thinking items,
rated on a 0–4-point scale. For each item, respondents are asked to “indicate how
often they have been aware of thinking a particular thought on occasions when they
have noticed the tinnitus”. The negative items are scored from 0 to 4, whereas the
positive items are scored from 4 to 0. The total score is the sum of the scores of each
item and ranges from 0 to 104. A high score represents a greater tendency to engage
in negative cognitions in response to tinnitus and low engagement in positive
cognitions.
Regarding general stressor identification, we adopted the CAPPE questionnaire
[16] that investigates the presence of different kind of stressors: chemical (pro-
longed expositions to solvents, assumptions of ototoxic drugs), acoustic (noise
exposure, acoustic neuroma, otosclerosis, hearing loss), pathologies (diabetes,
thyroiditis, autoimmune diseases), physical (professional stress, worsening of tin-

nitus during physical exercises) and emotional (sleep disorders, job change,
depression).
The general perceived stress (due both to WAST, general health and life condi-
tions) is quantified through the Perceived Stress Questionnaire (PSQ) [17]. It is
designed to represent the subjective perspective of the individual (“You feel…”).
Because stress results from an overload of experienced unpredictability and uncon-
trollability of events, the existence of stress in a subject is partially inferred from
information on the person’s experience of lack of control. The presented stress
experiences in PSQ were intended to be abstract enough, to be applicable to adults
of any age, stage of life, sex or occupation, but at the same time interpretable as
specific to a variety of real-life situations. For example, “you feel under pressure
from deadlines” could refer to anything from a payment to an oncoming birthday
party or to a grant proposal. This questionnaire asks the respondent how often cer-
tain experiences of stress occurred in the last month. The content of the items is not
referred to tinnitus, but it focuses on a more cognitive appraisal of stress. PSQ is a
20-item questionnaire of 4 scales, each resulted with 5 items:
• Scale 1 (worries) covers worries, anxious concern for the future and feelings of
desperation and frustration (e.g. “you have many worries”).
• Scale 2 (tension) explores tense disquietude, exhaustion and the lack of relax-
ation (e.g. “you feel mentally exhausted”).
• Scale 3 (joy) is concerned with positive feelings of challenge, joy, energy and
security (e.g. “you are full of energy”).
• Scale 4 (demands) covers perceived environmental demands, such as lack of
time, pressure and overload (e.g. “you feel you are in a hurry”).
Each positive (yes) answer to scales 1, 2 and 4 is scored 1 point. In joy scale the
score is 1 point for each negative (no) answer because all items of this scale are
positively worded. Thus, maximum possible score means that the most unbearable
stress perception is 20: the higher the total score, the higher the perceived stress.
14.3 Identification of Treatable Patients
The inclusion criteria are:

1. Acute or chronic tinnitus with TRQ less than 80.
2. CAPPE’s item “increasing with physical exercise” with a positive answer.
3. PSQ score at least 15 as total score OR 4–5 score in “tension” subscale.
4. Patient’s tinnitus modulated by somatic manoeuvres as described above.
5. No tinnitus modulation by the Jendrassik manoeuvres. In our experience
modulation by clenching, neck forceful flexion, etc. AND Jendrassik modulation
mean a no-specific facilitation of tinnitus perception to be distinguished from
specific, treatable, somatic involvement.
6. Trigger or tender point in the muscles, specifically activated during forceful
somatic manoeuvres, e.g. the masseter or anterior temporal regarding clenching
and sternocleidomastoid regarding neck flexion or rotation.
Feldman masking curve, LDL level, TRQ, PSQ and TCQ represent the outcome
measures.
14.4 Treatment
WAST treatment is mainly based on the so-called Tinnitus School as described

elsewhere [18–20]: Tinnitus School is a five-step programme as follows:
1. Amelioration of lifestyle through adequate counselling based on the case history
and CAPPE questionnaire.
2. Removing cervico-cephalic sensory–motor disturbances, by means of Manual
Medicine techniques (Maigne and Nieves [13]; see dedicated chapters) including
also high-velocity low-amplitude vertebral manipulations directly performed by
the physician.
3. Leading the patient to an awareness of own body and learning breath and neck
tension control, through physical exercises performed with a physiotherapist in a
gymnasium (Table 14.2). Tinnitus School physiotherapy programme is consti-
tuted by ten sessions subdivided into three sessions per week along 2 weeks
followed by two sessions per week along two other weeks. The first step is to
prepare the patient to cooperate in a complex programme involving movement,
thinking and learning. Muscle–skeletal impairments are often provoked by or
associated with tension and anxiety; that is why head and neck disorders have to
be treated before training. Therefore, it is more necessary to begin treatment with
simple relaxation exercises to manage patient’s tension. Physical exercises are
pointed to postural control because, in chronic somatic tinnitus as well in WAST,
the abnormal alignment of body parts with respect to each other and to the base
of support may be due to both muscle–skeletal cervico-cephalic impairments and
changes in patient’s internal perception of the own sensations induced by patho-
logical attention to tinnitus. Simple exercises have to be planned, and they are
generally pointed to mobilization of the pelvis, of the cervical rachis and of the
thoracolumbar spine. In some cases massages can be useful either to relax the
patient or to mobilize joints, including slow-velocity high-amplitude vertebral
manipulations performed by the physiotherapist.
4. Shifting patient attention away from tinnitus, through home physical exercises
(Table 14.3).
5. Bibliotherapy. Self-help books exist for a wide variety of psychological prob-
lems. Studies of their value indicate that they can help individuals to make
substantial improvements [21], on average about as much as psychotherapy.
We propose to our patients the Italian version (Springer, Milan, 2012) of
Tinnitus: A Self-Management Guide for the Ringing in Your Ears. This self-
help book by Henry and Wilson [22] is based on the cognitive–behavioural
principles, including educational information on tinnitus, cognitive reappraisal
and restructuring, relaxation and stress management techniques, attention
control techniques, use of self-instruction, making lifestyle changes and main-
taining gains.
Table 14.2 Tinnitus School Gymnasium Training Protocol
Supine (all the exercise are performed with patients’ head comfortably lying on a pillow)
• Relaxation exercises with control of breathing, improving consciousness of abdominal
or thorax breathing: deep inhaling followed, after few seconds, by a forced exhaling
while pronouncing the word “one”. This exercise is repeated 8–10 times
• Patients move the head first slowly and then faster in all directions, focusing on a target
straight on the ceiling
• Patients take the right knee against the chest, then extend the leg and take the left knee
against the chest. A gentle traction of the flexed leg is performed by the patient himself
when the knee is taken against the chest
• Patients take both knees to the chest, simultaneously helping gently with the hands
• Patients lift the pelvis taking the arms extended over the head. Then patients retake the
arms along the body lowering the pelvis
• Patients grasp a stick. Then they extend the arms over the head and then return in the
primary position
• In the quadrupedal position, patients inhale and arch the back while taking the head
between the arms. Then they exhale while retroflexing the head and rotating the pelvis
in hyperlordosis
• In quadrupedal position, patients extend simultaneously the right arm and the left leg,
repeating the same exercise with the left arm and the right leg
• In prone position, patients lift their left arm and the right leg, maintaining the forehead
over the bed, repeating it with the right arm and the left leg
Sitting
• Patients move the head first slowly and then faster in all directions, focusing on a target
straight in front
• Patients look for three targets sited, respectively, in front, at their left and at their right.
Then patients focus on the front target, and then they move the head, focusing on the
right-sited target. At last they rotate leftward the head, maintaining the focus on the
right-sited target
• Patients focus on the frontal target. Then they move the head leftward and focus on the
left-sited target. At last they rotate rightward the head, maintaining the focus on the
left-sited target
• Patients turn the head rightward and focus on a target on the lateral wall. Then they are
instructed to move the head straight, maintaining focus on the target, through eye
counterrotation, and count until 10
• Patients turn the head leftward and focus on a target on the lateral wall. Then they move
the head straight, maintaining focus on the target, through eye counterrotation, and
count until 10
• Patients extend their right arm and lift their thumb. Thus, patients move slowly the arm to
and fro before along a horizontal direction and then along a vertical direction. Patients
pursuit the thumb with eyes only, first slowly and then increasing progressively the
velocity of thumb displacement
• As above but moving simultaneously also the head, trying to maintain the eyes still
• Patients grasp a stick with both hands and take the stick behind the shoulder, positioning
the stick at the level of cervico-dorsal junction. In this position they rotate to and fro the
trunk, maintaining the head still also focusing on a target straight in front. Rotation of
the trunk has to be harmonic with quiet breathing
• Patients put the stick forward on the sternum at the level of the sternoclavicular joint.
Then they perform rhythmic backward displacements of the shoulders
• In this position they rotate to and fro the trunk, maintaining the head still also through
fixation of a target straight in front. Rotation of the trunk has to be harmonic with quiet
breathing
• Paying attention to quiet breathing, patients inhale. Then, exhaling, they bend forward,
taking the head on the right knee. They wait for 10 s. Then, inhaling, they return in
sitting position
• Paying attention to quiet breathing, patients inhale. Then, exhaling, they bend forward,
taking the head on the left knee. They wait for 10 s. Then, inhaling, they return in sitting
position
• Patients inhale. Exhaling, they bend forward to keep an object on the floor. Then they
inhale and take it up over the head and then they fixate it for 10 s. Patients inhale.
Exhaling, they bend forward and take the object on the floor
Standing
• Patients focus themselves on a mirror and align correctly their posture. Thus, they
maintain quiet equilibrium for 1 min, paying attention to breathing, before they
maintain their eyes open and successively they close their eyes, imagining the correct
position in their mind. They remain in this position for at least 1 min, paying attention
to breathing. Then they oscillate to and fro according to the breath rhythm, hearing the
air that enters and then exits from the lungs
• Patients in quiet upright position fixate a target on a mirror. In this case they have two
planes of fixation: the target and their image. Thus, they have to be able to extract the
correct fixation information from visual inputs. Then they oscillate to and fro according
to the breath rhythm, hearing the air that enters and then exits from the lungs
• Patients keep a little object and lift it over the head, fixating it. Then they deeply inhale.
Exhaling, they bend forward, placing the object on the floor. They wait for 10 s and then,
inhaling, they lift again the object over the head
• Patients take a little object over their head. Maintaining the object, they move it in small
circles according to breath rhythm, hearing the air that enters and then exits from the
lungs
Table 14.3 Tinnitus School Home Training Protocol
Supine
• Relaxation exercises with control of breathing, improving consciousness of abdominal
or thorax breathing: deep inhaling followed, after few seconds, by a forced exhaling
while pronouncing the word “one”. This exercise is repeated 8–10 times
• Take your two knees to the chest, simultaneously, helping, gently, with the hands
• Lift your pelvis while taking simultaneously your arms extended over your head. Then
retake your arms along the body while lowering your pelvis
• Grasp a stick. Take your extended arms over your head and then return in the primary
position
• In prone position lift your left arm and your right leg, maintaining your forehead over
the bed. Then repeat with the right arm and the left leg.
Sitting
• Move your head first slowly and then faster in all directions, focusing on a target
straight in front of you
• Grasp a stick with both hands and take the stick behind the shoulder, positioning the
stick at the level of the cervico-dorsal junction. In this position rotate to and fro the
trunk, maintaining the head still also through fixation of a target straight in front.
Rotation of the trunk has to be harmonic with quiet breathing
• Repeat the exercise, putting the stick forward on the sternum at the level of the
sterno-clavear joint. Then perform rhythmic backward displacements of shoulders
Standing
• With your hands on a table, lift yourself on your tiptoes and maintain this position for
30 s. Pay attention to breathing!
• With your hands on a table, lift yourself on your heels and maintain this position for
30 s. Pay attention to breathing!
• Focus yourself on a mirror. Then oscillate to and fro, right and left, around your ankles
while keeping your pelvis still, according to breath rhythm, hearing the air that enters
and then exits from the lungs
• Repeat with your eyes closed
• Keep a little object and then lift it over your head and focus on it. With your extended
arms move it over and over wide circles, maintaining focus on the object, according to
the breath rhythm, hearing the air that enters and exits from the lungs
• Repeat with your eyes closed. Pay attention to breathing!
• Keep a little object and lift it over your head. Focus on it. Inhale. Then exhale and bend
yourself forward, taking the object on the floor. Wait for 10 s and then, inhaling, lift
again the object over your head. Pay attention to breathing!
14.5 Outcome
Decreasing TCQ, TRQ and PSQ scores represents a significant improvement in the
quality of life of the patients; thus, generally speaking, WAST treatment results in a
significant decrease of tinnitus disturbance (TRQ and TCQ) through a decreased
perception of stress (PSQ). A strict selection of the subjects and patients strongly
motivated “to feel better” is needed.
Tinnitus, in general, may represent a sort of auditory after-effect [23–25]: an
interrupted sound can be perceived as continuous when noise masks the interrup-
tion, creating an illusion of continuity. It is reasonable to assume that WA somatic
disturbances convey abnormal inputs on DCN, creating something like spinal seg-
mental sensitization described by Fisher [26] to explain chronic myofascial pain.
According to this idea, somatic inputs may represent the “sensorial noise” in the
DCN that masks the interruption, creating an illusion of continuity, continuity that
we know to be the prerequisite for inducing chronic tinnitus at both cortical and
limbic level.
References
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Audiol 23:53–62
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Tinnitus J 1:115–126
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management. CRC Press, Taylor & Francis Group: Boca Raton FL. ISBN 0-8493-3121_8
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2(2):111–114
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ferent clinical and healthy adult samples. Psychosom Med 67(1):78–88
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Otorhinolaryngol Relat Spec 68(1):31–36
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management based on a stress-reaction tinnitus model. Int Tinnitus J 13(1):63–68
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Part III
Evaluation
Anamnesis and Clinical Evaluation
of Whiplash-Associated Equilibrium 15
Disturbances (WAED)
A. Cesarani, D.C. Alpini, D. Brambilla,

and F. Di Berardino
15.1 Introduction
In all medical fields a good case history evaluation is the key of a correct diagnostic
pathway. Patients’ complaints have to be documented as completely as possible just
from the beginning of the disease. Sometimes the examiner uses technical terms to
question the patient, and this can lead to confusion and misunderstandings. The first
diagnostic task is to differentiate between vertigo and dizziness or disequilibrium,
ruling out the many varieties of indistinct dizziness such as faintness. Vertigo is
linked with a spinning sensation around the head and frequently a vestibular disor-
der. Vertigo is the awareness of some dysfunction in the balance mechanisms, that
is, a dysfunction in the balance mechanisms becomes a conscious experience. The
sensation is characterized by feelings of “spatial disorientation”, whereof the illu-
sion of false movement is the most characteristic. “Rotatory sensation” is the most
typical sensation, but it is not the sole feeling generated by balance dysfunction. The
basic impression has to be the sensation of loss of stable subjective relationship with
the environment. In this way less typical sensations must be included and are called
“atypical” vertigo. On the other hand, syncopes, blackout, drop attacks, odd
sensations in the head, etc., have to be denied as primary “vertigo” sensations, but
A. Cesarani • F. Di Berardino
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
D.C. Alpini (*)
D. Brambilla
Department of Otoneurology, IRCCS “E. Medea”, “La Nostra Famiglia” Association,
via Don Monza 20, Bosisio Parini, Italy
e-mail: daniele.brambilla@bp.lnf.it

Fig. 15.1 Grateu’s synoptic diagram for anamnesis
they can accompany true vertigo. Dizziness or a turning sensation inside the head
may result from disturbances of integrating structures within the central nervous
system. Atypical dizziness is usually confused with disequilibrium. The term “diz-
ziness” is used popularly. It includes a multitude of symptoms related to the vestibu-
lar system or other aspects of the nervous system. Dizziness is applied to physical,
emotional or intellectual disturbances, whose common denominator seems to be a
loss of stability, a disruption of the pattern in which the individual is aware of his
surroundings and their relation to him, whether these refer to his physical orienta-
tion in space, his emotional equilibrium or his intellectual clarity. It is important that
the patient describes symptoms with his/her own words in the simplest way. In this
sense Grateu [1] proposed a simplified chart to investigate vertigo and dizziness
during common or less common daily activities (Fig. 15.1) every time the examiner
has to lead the patient in order to identify the main elements of patient history.
In equilibrium disturbances particular attention has to be pointed on qualitative
and quantitative aspects of symptoms.
15.2 WAED Anamnesis
The following aspects have to be investigated:

• Vertigo or dizziness. It is important to determine which symptom is prevalent or
if both are present or if there is a particular and recurrent sequence between ver-
tigo and dizziness. For example, after a whiplash injury, dizziness appears when
the patient removes the collar, performing normal activities, while vertigo
appears during rotation or flexo-extension of the head.
15 Anamnesis and Clinical Evaluation 155
• Onset of the symptoms. Immediately after whiplash, or the day after, or when the
collar was removed, or when physiotherapy began.
• Direction of vertigo rotation or the side of prevalent unsteadiness.
• Remission with particular position of the head/neck.
• Combination with spine pain and stiffness, with brachial paresthesias, with dys-
phagia or dysphasia, with neurovegetative symptoms such as nausea and vomit-
ing, with cognitive symptoms such as amnesia and attention disturbances and
with auditory symptoms such as hearing loss and tinnitus.
• Loss of conscious or combined with vertigo/dizziness.
• Headache and/or migraine immediately after vertigo attack or in the following
days/weeks/months.
• Incidence of symptoms on daily life activities. These qualitative aspects of
symptoms can be quantified using activities of daily living (ADL) questionnaires
[2]. As with functional scales, there is a tendency to use different standards,
depending on the type of lesion one aims to study. However, the usefulness of
questionnaire and ADL estimations should not be underestimated. The clinician
may well use this expertise to enhance the objective assessment of the patients.
However, such estimations may be biased, and they cannot easily be quantified
or documented for studies or evaluation of the effect of treatment. To get better
objective estimations, several functional scales have been developed, generally
designed for the study of a certain group of patients, thereby lacking the quality
of general applicability. Well-known scales are the Tinetti [3] and the Berg
Balance Scale [4, 5].
• Temporal distance between any first medical visit and whiplash.
• Temporal onset of each symptom and reciprocal combination.
• Frequence of spontaneous attacks.
• Intensity that can be quantified on a decimal scale.
• Duration: continuous, subcontinuous, transient, recurrent.
• Temporal correlation with hearing disturbances: no hearing disturbances, hear-
ing symptoms before, during and after vertigo attacks, etc.
• Accident aspects
– Whiplash of the driver or the passenger.
– Anterior or posterior passenger.
– Safety belts.
– Rear-end or lateral or diagonal collision.
– Collision with resting or moving car.
– Position of the head during injury. For example, if the passenger, with safety
belt, was speaking with the driver with the car stopped for a traffic light, then
a pure rear-end collision would not induce a pure sagittal antero-retroflexion
of the head but rather its torsional movement with the fulcrum on the first
thoracic vertebra and with a torsion of the trunk with the fulcrum on the first
lumbar vertebra. Such a complicated injuring mechanism usually induces
stronger longer-lasting symptoms, sometimes with severe vertigo and
dizziness.
The prognosis of WAED depends on concomitant diseases and/or previous ves-
tibular disorders. Thus, it is important to investigate:
• Vertigo or unsteadiness months or years before whiplash

• Previous trauma
• Previous otoneurological visit/examinations either for symptoms or for working
capability evaluation
• Previous auditory disorders
• Heart or brain or vascular diseases
• Hormonal disorders such as dysmenorrhoea or dysthyroidism
• Metabolic disorders such as diabetes
• Use of alcohol, drugs and tobacco products
• Exposure to solvents or other cerebro-toxic factors
• Epilepsy
• Previous treatment for scoliosis or orthodontic problems which could influence
postural system compensation possibilities
• Kinetosis
During anamnesis the modality by which the patient tells his own history can
suggest to the clinician some other characteristics, such as anxiety, restlessness or
depression. Sometimes specific psychometric scales can be used, but they are gen-
erally noises and not well accepted to the subject. Computerized anamnestic sys-
tems, such as NODEC elaborated by Claussen [6], are very useful in order to
standardize the series of questions, but it reduces the interpersonal interaction
between clinician and patient. Generally speaking we can say that computerized
anamnestic systems are particularly indicated for medicolegal expertise, while per-
sonal anamnesis is more useful in the treatment planning. The clinician has to iden-
tify psychological symptoms due to the stress and consequent symptoms. During
anamnesis the examiner can, if necessary, simply evaluate attentional disturbances
with easy temporal orientation (number of the present day), cultural (name of the
Popes), memory (series of numbers) and logic reversal ability tasks.
A useful questionnaire is the Dizziness Handicap Inventory proposed by Jacobson
and Newman [7] whose short form has been recently developed by Tesio et al. [8].
DHI investigates multiple aspects of activities of daily living and their correlation
with evocation of equilibrium disturbances (Table 15.1). The short form is a simpli-
fied questionnaire which has been proved to be as reliable and accurate as the long
form (Table 15.2). The questions are not restricted to the patient’s problem (vertigo
and dizziness), but they investigate the patient as an entire person. For example, it is
possible that vertigo and dizziness don’t cause difficulties in reading (answer “no”
in DHI), but the patient may have a vision impaired for ophthalmological problems.
In this way the correct answer in the DHIs will be “yes” because in every way read-
ing is difficult and impaired vision, for any cause, may impair balance.
In elderly WAED the increased risk of falls may be quantified through the
“Falling Risk Inventory” [9].
15.3 Clinical WAED Patient’s Examination
As we said in the Introduction, whiplash is a true noncontact cerebral trauma. Thus,

the otoneurological and equilibrium examinations have to evaluate some neurologi-
cal, orthopaedic and psychiatric aspects.
Table 15.1 Dizziness Handicap Inventory
Instructions: The purpose of this scale is to identify difficulties that you may be
experiencing because of your dizziness or unsteadiness. Please answer “yes”, “no” or
“sometimes” to each question. Answer each question as it pertains to your dizziness or
unsteadiness problem only.
Does looking up increase your problem?
Because of your problem, do you feel frustrated?
Because of your problem, do you restrict your travel for business or recreation?
Does walking down the aisle of a supermarket increase your problem?
Because of your problem, do you have difficulty getting into or out of bed?
Does your problem significantly restrict your participation in social activities such as
going out to dinner, going to movies, dancing or parties?
Because of your problem, do you have difficulties in reading?
Does performing more ambitious activities like sports, dancing and household chores
such as sweeping or putting dishes away increase your problem?
Because of your problem, are you afraid to leave your home without having someone
accompany you?
Because of your problem, have you been embarrassed in front of others?
Do quick movements of your head increase your problem?
Because of your problem, do you avoid heights?
Does turning over in bed increase your problem?
Because of your problem, is it difficult for you to do strenuous housework or yardwork?
Because of your problem, are you afraid people may think you are intoxicated?
Because of your problem, is it difficult for you to go for a walk by yourself?
Does walking down a sidewalk increase your problem?
Because of your problem, is it difficult to concentrate?
Because of your problem, is it difficult for you to walk around your house in the dark?
Because of your problem, are you afraid to stay at home alone?
Because of your problem, do you feel handicapped?
Has your problem placed stress on your relationships with members of your family or
friends?
Because of your problem, are you depressed?
Does your problem interfere with your job or household responsibilities?
Does bending over increase your problem?
15.3.1 Cranial Nerves
Generally, the olfactory nerve is not investigated routinely also because it requires
necessary instrumental equipments (olfactometry). The optic nerve is clinically
investigated evaluating the fundus oculi by means of an ophthalmoscope. Extrinsic
and intrinsic ocular motilities have to be always investigated. During oculomotric-
ity, extrinsic evaluation smooth pursuit and saccadic eye movements have to be
investigated using a pen or the examiner finger as target. Also the sensitivity of the
face (trigeminus) and corneal reflexes has to be evaluated. Regarding the facial
nerve, mimic aspects are sometimes evident, and dysesthesias of the auditory exter-
nal meatus have to be searched. The Schirmer test can complete facial examination.
The auditory function must be more correctly investigated with the different
Table 15.2 Dizziness Handicap Inventory Short Form
Instructions: The purpose of this scale is to identify difficulties that you may be
experiencing that can cause your dizziness or unsteadiness. Please answer “yes” or “no”
to each question even if disturbances are caused by problems different from vertigo,
dizziness and unsteadiness.
Does looking up increase your symptoms?
Do you restrict your travel for business or recreation?
Do you have difficulty getting into or out of bed?
Do you have difficulties in reading?
Do you avoid heights?
Is it difficult for you to go for a walk by yourself?
Is it difficult for you to walk around your house in the dark?
Are you afraid to stay at home alone?
Are you depressed?
audiometric tests, leaving the diapason tests to the history. Only the Weber test can
be sometimes useful during clinical investigation. The inspective visit of the mouth
and the larynx allows a complete evaluation of the IX, X and XII nerves, eventually
completed with stimulation of the external auditory meatus and posterior pharyn-
geal wall to induce, respectively, cough and pharyngeal reflexes. The XI nerve is
usually evaluated during postural examination, with palpation of the sternocleido-
mastoid and trapezius.
15.3.2 Posture
Several approaches may be used to estimate human postural control and they may
be considered complementary. Clinical investigation can yield valuable informa-
tion. The direct observation of patient behaviour, even during anamnesis, may con-
tribute information otherwise overlooked. Several generally well-known
examination procedures may be applied to help the examiner to evaluate the inves-
tigated subject. The use of standardized protocols also gives the examiner more
experience in interpreting the outcome of the procedures. The active and passive
movements of the head with respect to the neck, the trunk and the pelvis must be
estimated. Pain and movement limitations have to be noted and in a certain way
quantified. Palpations of the paravertebral extensor muscles, with special regard to
those of the neck and the back, have to be performed in order to appreciate hypo- or
hypertonus of the muscles. Simple muscular force test for the arm and leg extensors
is useful. With the patient in supine position, a Babinski test is simple and useful to
perform. General muscular tonus can be simply evaluated by asking to the patient to
resist with his/her thumb and index contacting them in a circle during an opposite
force of the examiner.
Tendon reflexes may be simply investigated. Trigger and tender points have to be
routinely searched along all paravertebral muscles, and temporomandibular joints
have to be inspected in static and dynamic (opening, protrusion, laterotrusion, etc.)
positions of the jaw.
During postural evaluation some sensorial evaluation can be contemporarily per-
formed especially if paresthesias are complained.
15.3.3 Eye Movements
Eye movements can be easily evaluated in a clinical manner and using instrumental
devices. In clinical practice the investigator is in front of the patient. First the exam-
iner lifts suddenly the right thumb in front of the patient (at about 50 cm from his
eyes) asking him to fixate it without moving his head, then he lifts the left and so on
the examiner continues lifting alternatively the right and left thumbs, and patient
continues fixating them, producing saccadic eye movements. The most important
features that can be noted are the latency of the eye movements and their conjuga-
tion. Also dysmetrias can be revealed because sometimes patients are not able to
fixate the thumb with only one saccade but they require adjustments of the eye
movements. Then the examiner asks to the patient to fixate his right thumb placed
at 50 cm from patient’s eyes, during a slow continuous to-and-fro movement. In this
case a smooth pursuit can be elicited. The most important feature that can be noted
is the regularity of the movement that must be continuous and harmonic.
15.3.4 Vestibulo-Ocular Reflex
Clinically, some information on vestibulo-ocular reflex (VOR) can be obtained by

turning the patient’s head while observing the optic disc during funduscopy. The
patient must be instructed to maintain fixation on an object across the room.
Normally, the disc remains steady in space, but if, say, the right labyrinth is hypoac-
tive, the disc will seem to jerk during turning of the head to the right. When the
vestibular loss is profound, this jerk eye movement in response to turns of the head
can be seen by the naked eye. In this case it is best to instruct the patient to fixate on
the examiner’s nose (so-called Halmagyi sign, named also as the head impulse test
or head thrust test) [10, 11].
Assessment of the otolith function clinically is even less easily done. Counter-
rolling of the eyes can be seen when the head is rotated to the ear down on to the
shoulder; the eyes slowly deviate in the opposite sense and then there is a rotatory
quick phase causing torsional nystagmus. This response is, however, mainly depen-
dent on the vertical semicircular canals rather than the otoliths. Skew deviation of
the eyes (vertical divergence of the eyes) without nystagmus is thought to reflect
tonic otolith pathway imbalance. It can be seen with utricular nerve lesion or with
lesions of the mesencephalon, especially those involving the interstitial nucleus of

Cajal and medulla; this type of tonic rotation can be suspected from a head tilt or the
eye covering test or seen from tilting of the optic disc.
Otolith-ocular reflexes may be investigated by means of a modified Halmagyi
test using a brisk but small translational impulse of the head: head heave test [12].
One of the cardinal signs of abnormal vestibular function is nystagmus.
Nystagmus (Ny) is a biphasic involuntary movement of both eyes (generally), and it
is constituted by a slow displacement of the eyes in a direction (slow phase of nys-
tagmus) followed by a rapid return of the eyes in the primary position of the gaze.
Nystagmus is classified according to the manoeuvres that are able to elicit it:
• Spontaneous nystagmus: it is present without any provocative manoeuvre.
Vestibular nystagmus is caused by an imbalance between the paired vestibular
structures. The nystagmus is called first degree if present only when gaze is
directed towards the fast phase, second degree if present in the primary position
or third degree if present when the eyes are deviated in the direction of the slow
phase. Removal of fixation typically enhances the nystagmus if the lesion is
peripheral and the eyes drift markedly towards the deranged side (fast phase
towards the healthy side). This can be seen clinically with Frenzel’s glasses that
have high-dioptre convergence lenses which allow a magnified view of the eyes
of the patient, without the patient being able to fixate due to the blur produced by
the lenses.
• Gaze-evoked nystagmus.
It is elicited by the eccentric position of the eyes that the patient has to maintain
for at least 20 s. It is called also gaze-evoked nystagmus. When bilateral, it is
usually a sign of central disorders due to a deficit of the central gaze neural inte-
grator localized in the medial vestibular nucleus and in the prepositus hypoglossi
nucleus.
• Positional nystagmus.
Nystagmus may readily be induced or, if already present, modified by changes in
position of the head. The conventional method is the Dix-Hallpike manoeuvre
[13]. In this, the patient sits on a couch and the examiner firmly grasps the head
which is turned 60° towards one shoulder. The patient is instructed to keep the
eyes open and to fixate the examiner’s forehead. The patient’s head is rapidly
lowered to below the level of couch and the eyes observed for any nystagmus.
After an interval of 30 s, if nystagmus is not found, or after the nystagmus ceases,
the patient is returned to the sitting position. Again, any nystagmus is normally
noted. The test is repeated if nystagmus is found to see if there is any adaptation.
After this, the test is performed with the opposite ear dependent. The variables
noted are latency to onset of nystagmus, its duration and adaptation, its direction
and, finally, associated symptoms. If any nystagmus is found after the Dix-
Hallpike manoeuvre, nystagmus has to be investigated in supine position, in head
hanging position and with briskly turning of the head to one side while the patient
is in the supine position. Typical benign positional nystagmus indicates a periph-
eral dysfunction, it presents a latency, and it is generally horizontal rotatory,
usually geotropic, fatiguable and adaptable. Although it is generally unilateral,
occasionally what seems to be bilateral benign positional nystagmus occurs.
Typical central positional nystagmus occurs in a wide variety of lesions, espe-

cially those involving vestibulocerebellum. Spontaneous vertical nystagmus,
either upwards or downwards, can often be modified by positional testing using
the conventional Dix-Hallpike manoeuvre or by placing the subject supine or
prone. If the nystagmus is increased in prone position, it is usually decreased
lying supine. Nystagmus induced by canal stimulation can also be profoundly
modified by alteration of position of the head, due to otolith/semicircular canal
interaction.
• Vibration nystagmus.
Mastoid or suboccipital stimulation by means of a 100 Hz vibration delivered by
a specific vibration apparatus [14] evoked a nystagmus when canals or maculae
are unbalanced. In whiplash patient is very frequent to observe nystagmus
induced only by paravertebral cervical stimulation of one side, generally by the
same side of more pronounced cervical muscle tension and pain, probably due to
overstimulation of the cervical muscle spindles.
• Cervical nystagmus.
It is due to the activation of the cervico-ocular reflex. It is elicited by the rotation
of the subject with the head still. This provokes a stimulation of the neck muscles
(stretching reflex), a stimulation of the vestibular nuclei and the elicitation of a
nystagmus directed towards the opposite side of body rotation. In normal sub-
jects nystagmus usually does not appear, thus the gain of the COR has been cal-
culated to be very low (about 0.1). In patients cervical nystagmus can be more
easily observed especially when the labyrinth is hypofunctional.
• Head-shaking nystagmus.
In some patients vigorous head shaking may generate a nystagmus that is not
clinically apparent. The head-shaking test (HST) (20–30 full cycles at around
2 Hz followed by Frenzel’s glasses observation) is a useful addition to the clini-
cal vestibular examination.
• Optokinetic nystagmus.
Optokinetic nystagmus (OKN) is a nystagmus elicited by the rotation of the envi-
ronment with respect to the patient. It is a compensatory movement of the eyes
to pursue a target displacement more width than the visual field. It can be assessed
at the bedside with a small stripped drum rotated in front of the patient. This is
basically a pursuit task and not surprisingly correlates well with other pursuit
measures.
15.3.5 Otolith Function
Some patients attending WAE disturbances clinics report symptoms of unsteadiness

which suggest involvement of otolith rather than semicircular canal function. This
may include a sense of bobbing up and down, being carried upwards and down-
wards in a lift, or lateral and sagittal pulsions. Certain disorders of head and eye
coordination – for instance, the ocular tilt reaction combining head tilt and ocular
skew deviation – are thought to be due to interruption of central graviceptive oto-
liths pathways.
15.3.6 Stance
Most common human activities require the ability to stabilize the human body in
upright stance, to counteract perturbations and to allow voluntary movements,
according to gravitational forces. The standing human is an unstable physical struc-
ture. To counteract the effects of gravity and comply with the requirements to stabi-
lize the body during voluntary movements, there is a continuous modulation of
motor activity, especially in the so-called antigravity muscles, based on the also
continuously changing afferent sensory information. The postural control of the
standing human can therefore be considered in part a dynamic feedback control.
Furthermore, based on experience and visual information, the standing human may
foresee perturbations or changing requirements in advance, thus adding a substan-
tial degree of anticipatory or feedforward control. To evaluate the significance on
postural control of observations or test results, it is necessary to bear in mind the
physiological background and ability to maintain upright stance.
Regarding the clinical evaluation of stance, the classical Romberg test is easily
applied even in the office and may yield some information. A patient unable to per-
form a Romberg test will probably have prominent difficulties in everyday life.
During this test particular attention has to be paid to direction of the slow falling
rather than the fast compensation. The Romberg test with feet in tandem position
seems less appropriate as it requires a better than ordinary postural control and will
yield a high degree of false-positive results. A Romberg test with the neck extended,
however, may contribute further information. In this position the lateral semicircu-
lar canal is brought into line with the gravity vector. A patient with a vestibular
lesion causing ataxia and nystagmus falls in the direction of the slow phase of nys-
tagmus, while a patient with a cerebellar cause may fall towards the fast phase or the
slow phase depending on the site of the lesion. According to Magnusson [15] a
combination with the clinical headshake test and Romberg test may be performed.
Nystagmus induced by a headshake test cannot differentiate between a CNS lesion
and a peripheral vestibular lesion. One may, however, increase the sensitivity in
tests of stance by combining the headshake test with a Romberg or a stepping test.
The patient does headshakes for 10 s, standing with his back against a wall and then
rapidly taking four steps forwards. If there is an evident deviation or fall towards the
side of the fast phase of nystagmus induced by a previous headshake test, this may
be taken as suggesting a posterior fossa lesion. Patients with compensated periph-
eral vestibular lesions seem to deviate only slightly.
15.3.7 Gait
Gait is certainly one of the most complex functions in which the equilibrium system
must interconnect with inself and outself in order to provide a harmonious and coor-
dinate progression of the body into the environment.
Gait can be evaluated either under a clinical point of view or by means of sophis-
ticated equipments.
In order to investigate in clinical practice equilibrium control of gait, the patient

has to walk quietly in a large room to-and-fro before with eyes open and then with
eyes closed. Gait with eyes open provides generic informations regarding neuro-
logical aspects of gait.
Gait with eyes closed provides specific informations regarding the equilibrium
system. Not only the direction of body deviation has to be noted but also the qualita-
tive characteristic of gait: the width of the base of support, the position of the arms
during gait, the presence of pendular synkinesias and the stability of the head.
A simple way to evaluate equilibrium control of gait is the investigation, with
eyes closed, of stepping, a simplified gait on place. Generally the patient is asked to
step for about one minute that it is equal to about 60–80 steps. During this time, with
eyes closed, a certain forward progression of the patient is observed. The same
characteristic of the gait can be revealed also during stepping: rotation of the step-
ping, body sway, coordination of the movement, width of base support, etc.
Conclusions
At the end of a complete anamnesis and a complete clinical otoneurological
examination, the clinician has all the elements to plan the required instrumental
tests. These cannot substitute for the clinical sensitivity of the examiner but have
to confirm, specify and document alterations of the equilibrium system. On the
basis of anamnesis and clinical examination, treatment planning can be generally
completely performed even if instrumental tests are often indispensable to moni-
toring the results of therapy.
References
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of balance in the elderly: validity and reliability of a measurement instrument applied to the
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tory measures of postural balance in an elderly population. Arch Phys Med Rehabil
73:1073–1080
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reliability but absolute reliability varies across the scale: a systematic review. J Physiother
59(2):93–99
6. Claussen CF (1992) Equilibriometric topodiagnosis as a basis of modern therapy of vertigo
and dizziness. Neurootol Newsl 1(1):7–24
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Arch Otolaryngol Head Neck Surg 116(4):424–427
8. Tesio L, Alpini D, Cesarani A, Perucca L (1999) Short form of the Dizziness Handicap
Inventory: construction and validation through Rasch analysis. Am J Phys Med Rehabil
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9. Alpini D, Kohen-Ratz R, Braun R, Burstin A, Tesio L, Pugnetti L, Mendozzi L, Sambataro G,

Cesarani A, Giuliano DA (2001) Falls in the elderly: the development of a risk questionnaire
and posturographic findings. Int Tinnitus J 7(2):105–108
10. Halmagyi GM (2005) Diagnosis and management of vertigo. Clin Med 5(2):159–165
11. Ulmer E, Chays A (2005) Curthoys and Halmagyi Head Impulse test: an analytical device.
Ann Otolaryngol Chir Cervicofac 122(2):84–90
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heave” stimulus. Ann N Y Acad Sci 942:95–113
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(Lond) 73(10):C149–C151
14. Ulmer E, Chays A, Brémond G (2004) Vibration-induced nystagmus: mechanism and clinical
interest. Ann Otolaryngol Chir Cervicofac 121(2):95–103
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Alpini D (eds) Equilibrium disorders: brainstem and cerebellar pathology. Springer, Milan, pp
52–59
Whiplash Effects on Postural Control
16
M. Magnusson and A. Hahn
The human ability to maintain upright stance in the presence of external

disturbances such as gravity or body-support surface motion has intrigued
researchers over the last century.
Interest arose from basic neuroscience [1] and from clinicians who diagnose and
treat balancing problems [2].
Furthermore, most common human activities require the ability to stabilize the
human body in upright stance, to counteract perturbations, and to allow voluntary
movements, according to gravitational forces. The standing human is an unstable
physical structure. To counteract the effects of gravity and comply with the require-
ments to stabilize the body during voluntary movements, there is a continuous mod-
ulation of motor activity, especially in the so-called antigravity muscles, based on
the also continuously changing afferent sensory information (Fig. 16.1).
The postural control of the standing human can therefore be considered in part a
dynamic feedback control [3]. Furthermore, based on experience and visual infor-
mation, the standing human may foresee perturbations or changing requirements in
advance, thus adding a substantial degree of anticipatory or feedforward control [4].
To evaluate the significance on postural control of observations or test results, it is
necessary to bear in mind the physiological background and ability to maintain
upright stance. Postural control cannot be considered a strictly hierarchical system
but rather is characterized by decentralized or local decisions in a way which allows
comparisons with the popular algorithms of neural networks. There is a substantial
amount of redundancy. The complementary relationships between the afferent ori-
entational information, i.e. the visual vestibular and somatosensory information, in
M. Magnusson (*)
Department of Otorhinolaryngology, Lund University Hospital,
Lund University, 221 85 Lund, Sweden
e-mail: mans.magnusson@med.lu.se
A. Hahn
3ENT Clinic, 3rd Medical Faculty, Charles University Prague, Prague, Czech Republic
e-mail: hahn@fnkv.cz

166 M. Magnusson and A. Hahn
Fig. 16.1 A schematic n

representation of human litio
Vo
postural control in quiet
stance. To maintain upright
Anticipation
position and stabilize the
body, there are continuously
changing visual, vestibular,
proprioceptive and
mechanoreceptive sensory CNS–integration
inputs. As the standing
human is an unstable physical
structure, there can be stable
static position. Stance is Motor
therefore maintained by command
dynamic feedback control
with contribution of
anticipatory or feedforward
information
Vision
Vestibular
Proprioception
Pressor info
postural control have been well known since the observations of Romberg in the
nineteenth century. However, the redundancies of the sensory systems or the central
nervous pathways should not be interpreted as the information from the different
sensory systems or neural pathways being equivalent and interchangeable.
Postural control is reactive and its task is body stabilization in the sense that the
body is prevented from falling over. This may apply to different desired body-
support (body on support) or body-space (body in space) orientations. Often, the
task is to maintain a desired body-space orientation for stabilizing a given eye or
hand work space. The balancing represents then the platform onto which volitional
(‘proactive’) self-movements are superimposed. The balancing is relatively simple
when it is restricted to the anterior–posterior, a–p, plane and when the body sway
angles are small. Then, the head, arms, trunk, and legs essentially form a rigid seg-
ment, or link, that tends to sway about an axis through the ankle joints: this situation
allows treating body biomechanics as a single ‘inverted pendulum’ [5]. This balanc-
ing is called the ‘ankle strategy’.
In some situations, the balancing involves the hips to various degrees, depending
on a number of factors such as disturbance magnitudes or restrictions of foot sup-
port or motor or sensory conditions (‘hip strategy’ [5]; then, in addition, the knees
may get involved. Very large disturbance magnitudes may even evoke ‘rescue reac-
tions’ such as steps, hopping, or holding with the hand. These reactions are then
usually superimposed on the ankle joint stabilization.
There is evidence emerging which suggests that in cases of lesions or loss of
information from one receptor or control system, another set of commands or
16 Whiplash Effects on Postural Control 167
strategy may be used to regain a sufficient postural control [6]. If so, there should be
possibilities to evaluate the effects and differences of various lesions and the applied
therapies.
The measuring and analysis of spontaneous or stimulus evoked sway is called
posturography.
16.1 Posturography Without Perturbations
Quiet stance is called unperturbed stance. However, the standing body as an inverted
pendulum is inherently unstable. Gravitational torque arising with its angular
excursions away from the ideal gravitational vertical tends to tip it over. Therefore,
gravity will here be considered an external stimulus.
Measurement of body movements to quantitatively and objectively evaluate
postural control and responses led to the development of different sets of posturog-
raphy. The basic concept depends on measurement of the forces actuated by the feet
against the ground, measured with a forceplate. The forceplate consists of force
transducers placed to pick up the distribution of forces which are vertical or
horizontal to the ground. The simultaneous recordings from several transducers
allow calculation of the moment produced by the standing human in different
directions and shear (or transitional) forces to normalize effects of weight of
different subjects.
The data may then be used to calculate the projection of forces against the
ground. Although body sway is generally characterized in terms of kinematic and
kinetic variables such as centre of mass (COM) rotation about the ankle joint and
centre of pressure (COP) shifts on the support surface, respectively, it is of utmost
importance to the understanding of posturography to realize that the recorded pro-
jection of all forces against the ground is not the same as a projection of the subject
centre of mass (or gravity) but just the centre of forces. The trace that is recorded is
thus not equivalent to movements, especially fast ones, but rather to the stabilizing
forces.
Different variables may be derived from the force measurements. The sway
amplitude, sway variance, of sway in either anteroposterior or lateral planes or sway
path, sway velocity, and sway area describing two-dimensional movements are
commonly used variables to evaluate postural competence [7].
The passive ankle joint stiffness is too weak to maintain the body upright during
quiet stance. Instead, quiet stance is controlled actively, which is reflected in a con-
tinuously changing ‘spontaneous’ sway. Power density plots of the sway exhibit a
clear preponderance at low frequencies [8]. The sway is not fully explained by inter-
nal motions due to heartbeat, breathing, etc., but appears to reflect mainly fluctua-
tions of the active torque. Possible sources are sensor noise, central processing
noise, and irregularities in actuator performance. Complete sway suppression
appears not to be a goal of stance control. As a result of the sway, the COM excur-
sion and the gravitational torque it evokes vary over time. This represents a sensory
stimulus that in turn evokes changes in active torque. The active torque stands out in
the COP as rapid variations [9]. Comparing experimental findings of such COM and
COP changes with corresponding simulations using a COM angle control model.
Although measurements of quiet stance may contribute to separation of groups

of subjects with different lesions, the normal variations are so wide that classifica-
tion of individual responses and, hence, clinical usefulness becomes ambiguous. To
master such shortcomings, different techniques to increase the demands on the
postural control are applied. The idea is that if there is a deficit in the postural con-
trol system that is not evident because of the redundancy and adaptability of the
systems, the deficit will become evident if further sensory information is lost or
distorted. The classical Romberg test uses evasion of visual clues to load the pos-
tural system. Likewise, posturography can be performed and results compared with
open and closed eyes. This is a standard procedure used in most test set-ups [10]. If
the increase of sway compared to normals is greater with open eyes than with closed
eyes, this might be taken as suggesting less effective use of visual clues and may be,
but not unequivocally, interpreted as a sign of decreased CNS function. A foam rub-
ber pad can be positioned between the feet of the subject and the forceplate to
reduce mechanoreceptor sensation from the soles of the feet and increase the
difficulties in stabilizing the body. The patient can be asked to place his head in
different positions to increase difficulties with vestibular cervical interaction.
The role of static posturography in body sway assessment still has a limited
clinical use because of its intrinsic high variability which does not permit a reliable
diagnosis. There are no reports concerning the intersubject coefficients of variation
(CV) of static posturography parameters in healthy subjects. In order to make static
posturography a reliable clinical tool, it is necessary to use parameters with a CV
lower than 15 %. It is possible using ‘sensory ratio’ formulas, like sensory integra-
tion tests of the EquiTest equipment, which is probably the most widespread
commercially available equipment that utilizes six sets of disturbed sensory infor-
mation to estimate a sensory integration set.
It is possible to calculate similar ‘sensory ratio’ with standard static posturo-
graphic equipments including values from the unstable condition on foam pads.
According to Di Berardino et al. [11], the most reliable parameters in static
posturography were given by the use of bilayer rubber foam pads. The CV of the
visual and vestibular percentages were about 10 %. Therefore, the lowest variability
suggests that these percentages derived from the ‘sensory ratios’ using bilayer foam
pads, together with somatosensory one that was about 14.4 %, are the most accept-
able parameters for clinical use. Furthermore, the role of ‘sway-related’ tests with
foam pads, proposed by Allum et al. [12], is fundamental in order to make static
posturography more useful.
16.2 Posturography with Induced Perturbations
Balancing is often investigated in response to three external mechanical stimuli,

which are body-support surface tilt, surface translation, and contact force (e.g. a
push or pull having impact on the body).
16 Whiplash Effects on Postural Control 169
To further load human postural control with the purpose of revealing deficits, the
standing subject may be exposed to different perturbations, and the responses to
recover quiet stance are evaluated.
In the T-Post system from Toennies, the subjects stand, leaning somewhat
backwards, and the platform then tilts and induces a further backward movement of
the body. The subjects have to move forward to avoid falling; latencies and
amplitudes of this movement can be combined with EMG recordings to estimate
response latencies. The method can detect movement and probe synergistic muscle
activity if combined with EMG. In the motor coordination test of the EquiTest, the
platform is either tilted or translated with different velocities, and the postural
reactions of the subject are measured.
Vibration toward the antigravity muscles induces a sensation of movement and
involuntary body movements [12]. This has been used to perturb the standing
human for diagnostic purposes, calculating vibration-induced body sway (VBS).
Patients with posterior fossa lesions are reported to have larger responses when
vibrated toward the neck muscles than the calf muscles, compared to subjects with
vestibular lesions. Vibration toward the calf muscles according to a pseudorandom
binary stimulus (PRBS) induces an on- and off-going perturbation which can be
used to estimate an input–output relation and model postural control, which allows
estimation of the so-called characteristic parameters of postural control. Comparing
these parameters, one can get an estimation of the postural control of the subject.
The use of these parameters can distinguish, for example, between an acoustic neu-
roma and an acute vestibular lesion and also distinguish subjects with cervical dis-
orders. Patients who recover from hemispheric stroke demonstrate remaining
differences in postural control when evaluated with those parameters [13].
A vestibular spinal perturbation may evoke both lateral and anteroposterior body
sway by galvanic stimulation of the vestibular nerves. Evaluation of these responses
may give further information in posterior fossa lesions, but so far clinical studies are
lacking. Visual stimulation inducing a sensation of small amplitude translatory
movements of the surroundings may induce perturbations in the anteroposterior
plane, which, not surprisingly, differs in subjects with cerebellar lesions [14]. The
effect of visual stimulation, however, may be dependent on attention and state of
mind, and different patterns of response may be assumed in normal subjects. So far
visually induced perturbations, with the exception of the so-called stabilized visual
frame in EquiTest measurements, have not been used in clinical routine to the
knowledge of the author [15].
References
1. Baloh RW, Honrubia V (2001) Clinical neurophysiology of the vestibular system, 3rd ed.
Oxford University Press, New York; Trauma, pp 322–332
2. Brandt T, Krapczyk S, Malbenden L (1981) Postural imbalance with head extension.
Improvement by training as a model for ataxia therapy. Ann N Y Acad Sci 374:636–649
3. Forth KE, Metter JE, Paloski WH (2007) Age associated differences in postural equilibrium
control: a comparison between EQscore and minimum time to contact (TTCmin). Gait Posture
25:56–62
4. Clark S, Riley MA (2007) Multisensory information for postural control: sway-referencing
gain shapes center of pressure variability and temporal dynamics. Exp Brain Res 310:
176–299
5. Nashner LM, Black FO, Wall C 3rd (1982) Adaptation to altered support and visual conditions
during stance: patients with vestibular deficits. J Neurosci 2:536–544
6. Riley MA, Baker AA, Schmit JM, Weaver EE (2005) Effects of visual and auditory short term
memory tasks on the spatio-temporal dynamics and variability of postural sway. J Mot Behav
37:311–324
7. Baloh RW, Jacobson KM, Beykirch K (1998) Static and dynamic posturography in patients
with vestibular and cerebellar lesions. Arch Neurol 55:649–654
8. Contarino D, Bertora GO, Bergmann JM (2003) Balance platform: mathematical modeling for
clinical evaluation. Int Tinnitus J 9:23–25
9. Di Fabio RP (1996) Meta-analysis of the sensitivity and specificity of platform posturography.
Arch Otolaryngol Head Neck Surg 122:150–156
10. Shumway-Cook A, Horak FB (1986) Assessing the influence of sensory interaction of balance:
suggestion from the field. Phys Ther 66:1548–1550
11. Di Berardino F, Filipponi E, Barozzi S, Giordano G, Alpini D, Cesarani A (2009) The use
of rubber foam pads and “sensory ratios” to reduce variability in static posturography
assessment. Gait Posture 29(1):158–160
12. Allum JHJ, Zamani F, Adkin AL (2002) Differences between trunk sway characteristics on a
foam support surface and on the Equitest1 ankle-sway-referenced support surface. Gait Posture
16:264–270
13. Horak FB, Henry SM, Shumway-Cook A (1997) Postural perturbations: new insights for
treatment of balance disorders. Phys Ther 77:517–533
14. Dehail P, Petit H, Joseph PA (2007) Assessment of postural instability in patients with
traumatic brain injury upon enrolment in a vocational adjustment programme. J Rehabil Med
39:531–536
15. Magnusson T (1994) Extracervical symptoms after whiplash trauma. Cephalalgia 14:
223–227
Static Posturography and Whiplash
17
P.L. Ghilardi, A. Casani, B. Fattori, R. Kohen-Raz,
and D.C. Alpini
17.1 Static Posturography
The quiet upright position (Stance) is controlled by three distinct sensorial cues
organs: visual, somatosensorial (from skin and pressure sensors in the feet) and
vestibular (mainly from otolithic maculae).
Posture is more stable when all the sensory systems operate. However, the weight-
ening of each cue is adjusted in the vestibular nuclei and cerebellum [xxx] according
to the surface, the environment and the task. SOT test (see part I) is designed to
investigate the specific weightening of different cues in stance control. The sequence
of posturographic test adopted is aimed to investigate postural interactions between
sensorial cues, ranging from complete sensorial control (eyes open standing on a
solid surface) to quite exclusively pure vestibular control (eyes closed standing on
foam). Inputs from the vestibular canals and somatosensory system stabilize posture
more effectively at higher frequencies of body sway, while visual and otolith-organ
signals are more effective at lower frequencies. The amplitude threshold for detec-
tion of body sway differs between senses: the somatesthesic senses have the lowest
threshold, vision the next and the vestibular system has the highest threshold.
Whiplash can affect the balance system through an involvement of one or more
of these structures:
1. The neck proprioceptors
2. The peripheral vestibular system
3. The central vestibular system
P.L. Ghilardi • A. Casani • B. Fattori

Institute of Otorhinolaryngology, University of Pisa, 56100 Pisa, Italy
R. Kohen-Raz
The School of Education, The Hebrew University of Jerusalem, Har ha-Tsofim,
Jerusalem, Israel
D.C. Alpini (*)

172 P.L. Ghilardi et al.
After whiplash, an abrupt increase in discharge from the neck proprioceptors,

usually asymmetric, might be generated by an overexcitation of the sympathetic
fibres related to the B receptors of the deep cervical erector muscles [1, 2].
Several studies have reported altered postural control in people with neck pain
and disturbances in static balance have been demonstrated [3].
Non-specific neck pain or whiplash-associated disorder (WAD) exhibit greater
postural instability than healthy controls, signified by greater COP excursions irre-
spective of the COP parameter chosen. In particular, COP excursions are particu-
larly increased in WAD compared to healthy individuals.
Further, the decreased postural stability in people with neck pain appears to be
associated with the presence of pain and correlates with the extent of proprioceptive
impairment, but appears unrelated to pain duration [4–6].
Post-traumatic vertigo is not a clinical entity, but this term refers only to the com-
mon aetiology of a heterogeneous collection of vestibular disorders. Even if there
are many convincing signs indicating the existence of anatomical and functional
connections between the neck and the vestibular system, the assessment of vertigo
after whiplash is extremely complex. No reliable clinical, electronystagmographic
or posturographic test exists to confirm the linkage between the neck trauma and the
vertiginous symptoms.
Keeping these observations in mind, static posturography could provide useful
information about the postural conditions of patients suffering from vertigo after
whiplash.
Before the introduction of computerized posturography (PG), the VSR was
studied using various tests (Romberg, Fukuda, Unterberger, Babinski-Weil, Ataxia
test battery, etc.) which nevertheless do not permit a quantitative and objective
study of postural function. Falls and difficulties in dynamic task, such as single-leg
stance with eyes closed, the step test, tandem walk on a firm and soft surface, stair
walking and the timed 10 m walk with and without head movement, have also been
reported [7].
Routinely, posturography (PG) recording is performed under two basic
conditions:
1. Patient standing on the platform with eyes open (EO)
2. Patient standing on the platform with eyes closed (EC)
Besides these basic tests to verify the presence of a latent postural disorder, other
destabilizing tests are usually employed. We use two types of examinations to
verify this:
1. Patient standing on the platform with EC and with the head in extreme retroflex-
ion (EC-HER)
2. Patient standing on the platform with EC immediately after head shaking
(EC-HST)
The parameters we can achieve from the computer elaboration are shown in
Table 17.1. An important difference between the PG and the older techniques for the
study of posture is that the former provides us with precise objective data which can
be compared throughout time for each patient and each with different pathologies of
balance.
17 Static Posturography and Whiplash 173
In this context, PG, performed with particular types of stimuli or provocation

tests, may identify a cervical origin of the dizzy symptoms. Through tests performed
with rotation (“cervical dynamic activation”) [8, 9], “head turned” [10] (Fig. 17.1)
and retroflexion of the head [11] (Fig. 17.2), it will be possible to obtain some infor-
mation on how cervical inputs can generate instability syndromes. However, posi-
tive results obtained with the above-mentioned tests must be evaluated within the
entire clinical context because they cannot be considered as pathognomonic.
Table 17.1 The main parameters and the graphic elaborations obtained by computer, the role of
the proprioceptive inputs in patients suffering from postural disorders
Parameters Graphic elaborations
X min, max, mean Displacement of pressure centre on X axis
X min, max, mean Displacement of pressure centre on Y axis
Velocity of the sway Its standard deviation is an index of the “homogeneity” of the postural
oscillations
Length L (mm) Total sway path of centre of pressure
Surface S (mm2) Is indicative of the precision of the system
L.F.S. Correlation function between L and S
Statokinesigram Area covered by the sway
Stabilogram Displacement on time of the sway for X and Y
Fast Fourier transform
Romberg’s index Ratio between the same value with EC and EO
This allows a quantification of the importance of the pressoreceptor system for balance and pro-
vides us with useful information for the management of rehabilitation treatment
Statokinesigram
a
–2.0 cm –1.0 cm
Ref.: platform Ref.: centre of gravity position
Fig. 17.1 (a–c) Patient suffering from vertigo from WI. (a) Normal result in EO. (b) The SKG is
abnormal when the head of the patient is rotated towards the right. (c) A similar pattern can be
observed with the head rotated to left

–2.0 cm –2.2 cm
–2.0 cm –3.3 cm
Fig. 17.1 (continued)
Armato and Ferri [12] published a study on 569 patients with whiplash, with or
without associated head injuries. Of these, 21 % had either normal vestibular func-
tioning or only static stabilometric alterations that were compatible with a modified
proprioception of the cervical spine.
Cobo et al. [13] investigated 99 women. Fifty-four women had suffered whip-
lash within 2 weeks and 45 were included in a healthy control group. Static
Statokinesigram
–2.0 cm –2.6 cm
Stabilogram
22.4
D 13.5
4.5 X mean
–0.3 mm
–4.5
–13.5
S
–22.4 –2 s
(mm)
22.4
13.5
A
4.5
X mean
–4.5 –50.0 mm
–13.5
I
–22.4
–2 s
Fig. 17.2 Patient suffering from WI. Above, the pathological SKG in EO-HER; below, the SBG
shows a prevalence of the oscillation on the anterior-posterior axis
posturography on a force platform was carried out in all study participants, by

means of the Romberg test in four sequential phases, using the postural sway area
as a dependent variable. The visual analogue scale (VAS) and Northwick Park
Neck Pain Questionnaire (NPH) were used to evaluate pain and function. Postural
sway area increased significantly in each of the consecutive phases in both groups.
The differences of the means of the postural sway area were statistically signifi-
cant in all Romberg phases (p = .009 to p = .000). No correlation was found between
postural sway area and VAS or NPH scores. There was a positive correlation
between the postural sway area standing on a thick foam cushion placed over the
plate with closed eyes and the number of days of transitory incapacity (r = 0.414;
p = .009).
Two groups of subjects have been studied by Nacci et al. [14]: Group A
included 90 subjects (age range, 17–73 years; mean age, 40.8 ± 12.6; 59 females
and 31 males) suffering from whiplash injury (Grades 1 and 2 of the whiplash-
associated disorders classification – WAD) and Group B comprised 20 subjects
(age range, 23–79 years; mean age, 42.8 ± 17.1; 10 females and 10 males) with
whiplash injury (Grades 1 and 2 of the WAD) associated with minor head injury
(14–15 in the Glasgow Coma Scale – GCS) [41]. All the subjects (n = 110) in the
study complained of a balance disorder (postural instability, uncertain gait,
vertigo, etc.) that had arisen after trauma. The vestibular-spinal reflex (VSR) in all
patients was investigated by means of static stabilometry using the S.Ve.P.
Amplifon System©. The stabilometric test (performed within 15 days of trauma,
like the vestibular test) was carried out with eyes open (EO), eyes closed (EC) and
closed eyes with head retroflexed (CER). To evaluate the role of cervical proprio-
ceptive afferences, the cervical interference index corresponding to the surface
(SCI) and to the length of the oscillations (LCI) was calculated from the percent-
age ratio between the S and L values when the eyes were closed and the head
retroflexed and the same parameter when the eyes were closed but the head was
erect, considering a value less than 120 as normal 43.
To eliminate any cases of simulation, stabilometry was performed twice within
the same session in EO, EC and CER (retest) 25. Moreover, to exclude exaggerated
or simulated postural behaviour, subjects who had intercorrelation stabilometric
recordings that appeared frankly sinusoidal and/or those who had over 2,000 mm
surface values in OE were excluded from the study (12 subjects) 25 44. None of the
subjects in Group A (n = 90) or Group B (n = 20) showed stabilometric recordings of
sinusoidal intercorrelation in all three tests (OE, CE, CER). As far as the altered
posturographic recordings are concerned, while there was no specific pattern in the
two groups, they were clearly pathologic, especially during CER. Both in OE and in
CE, there was an increase in the surface values and in those pertaining to shifting of
the gravity centre on the sagittal plane, which was even more evident during CER.
As far as the indices of cervical interference are concerned in Group A, there was
pathological SCI (n.v. < 120) in 59 cases (59/90; 65.6 %) and pathological LCI
(n.v. < 120) in 44 (44/90; 48.8 %). In Group B, 11 cases with pathological SCI
(11/20; 55 %) and 12 with pathological LCI (12/20; 60 %) were found.
Since vestibular compensation develops after whiplash, the postural performance
improves progressively, even if in certain patients a persistent backward displace-
ment of the pressure centre could be noticed [15]. Often it is only through
Fig. 17.3 (a–c) Patient Statokinesigram

suffering from UVL after a a
WI with EO (a) stabilometry Ref.: platform Ref.: centre of gravity position
is normal. Only with
EO-HST (b) can an
abnormality of SKG be
detected. With EO-HER (c)
postural stability shows a
marked worsening
–2.0 cm –4.3 cm
–2.0 cm –3.0 cm
–2.0 cm –4.3 cm
sensitization tests (EC–HST, EC-HER) that it is possible to detect latent static

postural deficiencies not evident in basic conditions (EO and EC) (Fig. 17.3) [16].
Moreover, the PG allows assessing when some patients have reached a normal
postural performance even retroflexion. Under these conditions a remarkable
increase in the oscillations on the Y axis and a displacement of the pressure centre
towards the critical side are detected (Fig. 17.4) [17].
a Statokinesigram
Ref.: centre of gravity position
Ref.: platform
–2.0 cm
–5.2 cm
43.5 Stabilogram
26.1
D
3.7
X mean
–3.7
–5.9 mm
–26.1
S
–43.5 –2 s
(mm)
43.5
A 26.1
3.7
–3.7 X mean
–50.0 mm
I –26.1
–43.5
–2 s
Fig. 17.4 (a, b) Patient suffering from PPV after WI. The SKG with OC-HER (a) is abnormal;
the SBG (b) shows a prevalence of the oscillation on the anterior-posterior axis
Nevertheless, it must be considered that the findings may be altered or modified

because of the combined actions of more than one degree of lesion.
Beside a definition of the postural damage, static PG allows visualizing and
quantifying the extent of the disease and the effects of therapy on postural behav-
iour in patients with VSR deficiency.
This observation has to be kept in mind in the case of patients suffering from postural
abnormalities following Wl in whom the posturographic test performed in EC-HER
plays an important role for evaluating the significance of the cervical proprioceptive
input at the base of the vertiginous symptoms. In this framework, PG seems to be very
useful for monitoring both postural deficiencies and the subsequent therapy.
Increased values of slow-sway component magnitude are evidenced in patients
with WAD despite of neck pain as assessed by Röijezon et al. [18].
In addition to the increase of postural sway that is more evident in anteroposte-
rior direction (Ruhe A review), a recent work has evidenced that, during balance
tasks with closed eyes and one-legged stance, the relative mean activity of the ante-
rior scalene, sternocleidomastoid, neck extensors and upper trapezius muscles,
expressed as mean relative activity related to maximum voluntary electromyogra-
phy (%MVE) measured by surface electromyography, was significantly increased
in WADs compared with healthy controls [19].
17.2 Tetra-ataxiametric Posturography
Tetrax system (Tetrax-IBS equipment by Sunlight Medical Ltd., Tel Aviv, Israel)
25–27 (CE patent n. 93741CE02; FDA establishment registration n. 3006701790)
consists of four independent mobile force plates, two for each foot. The plates are
positioned in order to measure any equilibrium disturbance from the two forefeet
and two heels. Each plate contains a strain-gauge force transducer, which is sensi-
tive to vertical force. Tetrax provides independent output from the four balance
plates and, by taking the average of all four measurements, provides a description
of body sway in terms of displacement of the patient’s centre of pressure. Subjects
are requested to stand quietly on the platforms in a quiet room in four different con-
ditions: eyes open and eyes closed on a solid surface and eyes open and eyes closed
on a foam pad in order to reduce somatosensorial and visual information [20–22].
The system measures the changes and fluctuations of the vertical force exerted
by the corresponding heel or forefoot during the default 30-s experimental time and
emits four separate wave signals at a sampling rate of 34 Hz. On the basis of these
fluctuations, the system computes a general stability score (ST), normalized for
body weight according to the following equation:
ST = t {S n1[( an − an − 1) 2 + ( bn − bn − 1) 2 + ( cn − cn − 1) 2 + ( dn − dn − 1) 2]}1/ 2/W

W.N
where a, b, c and d are the four pressure transducers, W is body weight, t is experi-
mental time and n is the number of signals sampled at 34 Hz.
Tetrax provides both quantitative and qualitative sway analysis.
17.3 Quantitative Sway Analysis
General stability (ST) is, therefore, calculated as an index, which refers to a mean
of oscillations, recorded by each plate: the higher the value, the lower the stability.
It is the quotient of the sum of the amplitudinal changes (body sway), recorded in
microvolts and divided by body weight. While it is not a direct measurement of
postural stability, the fluctuations of the vertical ground reaction force normalized
for body weight have been found to correlate with both the static and dynamic parts
of Berg’s balance test and with the anteroposterior centre of pressure (COP) veloc-
ity [28]. In fact, the ST score provides information about the adequacy of postural
adjustments. A lower ST indicates smaller fluctuations and therefore better postural
control, and it has also been seen to be significantly correlated to the equilibrium
score of the Equitest posturography system. The weight distribution index (WDI) is
calculated on the basis of the relative recorded weight at each of the four supports:
the higher the WDI, the higher the abnormal distribution of the weight that had to
be theoretically equally divided between the four supports.
17.4 Qualitative Sway Analysis
Fourier analysis of sway frequencies is a mathematical treatment of wave signals of

body oscillations on the horizontal plane produced by the patient in order to main-
tain an upright position.
The Tetrax system combines the signals from the left and right leg to result in
one sway frequency with a sampling rate of 34 Hz, as described by Kohen-Raz [23,
24]. The four signals recorded at the four sensors are analysed with the Fourier
transformation, and then Tetrax recalculates an average of the results obtained pro-
viding a unique parameter.
Fourier analysis is then carried out to determine which signal frequencies are
most common. Fourier analysis of sway frequency distribution shows that a normal
postural performance is characterized by a high intensity at the low range, and this
appears to indicate that posture is controlled with minimal effort, not involving any
activity of the semicircular canals, which are considered to be insensitive to body
displacements below 0.2 Hz.31 Fourier analysis of sway frequencies is divided into
eight frequency bands (F1–F8). Posturography with an interactive balance system
was recorded by means of equipment with four sensors; therefore, Fourier transfor-
mations were derived from four independent wave signals and were presented in the
form of a spectrum, broken down into the following eight frequency bands: F1
0.01–0.1, F2 0.1–0.25, F3 0.25–0.35, F4 0.35–0.50, F5 0.50–0.75, F6 0.75–1.00, F7
1.00–3.00 Hz and F8 above 3.0 Hz.
Previous studies on the Fourier spectral analysis of postural sway by Tetrax (25,
26, 30–33) have shown that typical ranges of postural frequency (i.e. frequency
bands) express the different levels of activity of postural subsystems, the systems
that affect postural sway. Study of postural frequency can provide insights into the
individual’s use of these postural subsystems, which include the vestibular,
somatosensory and other subsystems to maintain postural stability. Thus, spectral

analysis of postural sway might be a valuable tool in clinical diagnosis. Tetrax pos-
turography has been shown to have a high test-retest reliability.
Dehner et al. [25] investigated the balance control in patients with acute QTF
grade II whiplash injuries of the cervical spine by means of Tetra-ataxiametric pos-
turography in 40 patients with acute QTF grade II whiplash injuries and 40 healthy
matched controls. The stability index ST and the Fourier analysis FA (0.10–1.00 Hz)
were established for eight standing positions and sum scores were calculated. The
pain index was established using a visual analogue scale ranging from 0 to 100. A
follow-up examination was conducted for the patients after 2 months. The patients
with acute whiplash injuries of the cervical spine achieved significantly poorer
results for both ST and FA than the healthy controls. There were no differences
between the eight standing positions for both ST and FA. After 2 months, 17 patients
had no change in the pain development, 21 patients showed an improvement in pain
intensity and two patients had deteriorated. The subgroup of patients with improve-
ment in pain intensity showed a significant improvement in balance control con-
cerning the FA compared to patients with unchanged pain intensity. Authors
concluded that patients with acute whiplash injuries have a reduced balance control
as compared to matched controls. This study gives an indication that post-traumatic
neck pain is associated with impairments of postural control.
Kohen-Raz (unpublished data) coordinated a multi-country study in 90 chronic
WAD patients (Israel, Germany and Czech Republic) about Tetrax and WI. The
research was pointed to document backward displacement of COG following WI as
previously reported. Backward displacement is characterized, in Tetrax analysis, by
increasing of weight on the heels particularly evident during retroflexion of the
head. Heel weight displacement is due to whiplash-induced disruption of head-to-
trunk coordination that is necessary to maintain stability of ground projection of
COG during head movements: in normals when the head moves backward, the
trunk and the pelvis moves forward in order to counteract head displacement, while
in WAD patients this kind of coordination is lost. WAD patients were compared to
90 healthy subjects from the same countries. A Student’s t-test confirmed a signifi-
cant (p < 0.05) weight displacement on the heels in WAD patients with respect to
normals in the three countries when patients retroflexed their head.
17.5 Trunk Sway Measurement
In 2003 Allum et al. [26] proposed the use of body-worn sensors measuring angular
velocity (gyroscopes) or the acceleration of the trunk to effectively quantify balance
during stance and gait tasks to track improvements in postural control during recov-
ery from an acute unilateral peripheral vestibular deficit (UVL) and, successively, in
order to detect potential elderly fallers [27]. Postural control was quantified using
simple measurements of trunk sway: amplitudes of trunk sway angle and angular
velocity, in the roll and pitch directions as well as task duration, were examined for
a battery of stance and gait tasks. Sjostrom et al. [28] used the same device in WAD
patients. Trunk sway occurring during clinical stance and gait tasks was compared
between a group of subjects with a chronic whiplash injury, resulting from an auto-
mobile collision, and a normal collective. Twenty-five subjects with history of
whiplash injury and 170 healthy age-matched control subjects participated in the
study. Trunk sway angular displacements in chronic whiplash patients were assessed
for a number of stance and gait tasks similar to those of the Tinetti and Clinical Test
of Sensory Interaction and Balance (CTSIB) protocols. Data analysis revealed sev-
eral significant differences between the two groups. A pattern could be identified,
showing greater trunk sway for stance tasks and for complex gait tasks that required
task-specific gaze control such as walking up and down stairs. Trunk sway was less,
however, for simple gait tasks that demanded large head movements but no task-
specific gaze control, such as walking while rotating the head. They concluded that
subjects who have a chronic whiplash injury show a characteristic pattern of trunk
sway that is different from that of other patient groups with balance disorders.
Balance was most unstable during gait involving task-specific head movements
which possibly enhance a pathologic vestibulo-cervical interaction.
Vonk et al. [29] used trunk sway measured during several stance and gait tasks in
18 patients suspected of malingering in order to differentiate these from 20 patients
who had suffered unilateral vestibular loss 3 months earlier, 20 patients with docu-
mented whiplash injuries and 34 healthy controls. Classification results ranged from
72 to 96 % and were equally accurate for task or criteria variables based on 90 %
sway values. The tasks yielding the best discrimination were standing with eyes
closed on a foam and firm surface, standing with eyes open on a firm surface, stand-
ing on one leg and walking tandem steps. The criteria yielding the best discrimina-
tion were standing with eyes open on a firm surface, the difference between standing
with eyes closed on foam and firm surfaces, the difference between walking tandem
steps and standing on one leg with eyes open and the difference between roll and
pitch velocity when walking eight tandem steps. We conclude that discriminating
suspected malingering balance disorder patients is possible using variables or crite-
ria based on objective measures of trunk sway during several stance and gait tasks.
Findling et al. [30] showed a greater trunk sway for stance tasks and complex
gait tasks (e.g. walking up and down stairs) in patients with whiplash injury with
and without mild traumatic brain injury while they showed equal reductions in
trunk sway with respect to controls for simple gait tasks (e.g. walking while rotating
the head).
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Dynamic Posturography
18
S. Barozzi, B. Monti, D.C. Alpini, and F. Di Berardino
Different stable postures are possible according to the relative position of the three
principal muscle-joint systems – ankles, knees and hips – between the body’s COG
and the base of support (Fig. 18.1).
When external perturbations happen, the COG oscillates differently according to
the postural movement strategy adopted by each individual, depending on the
amplitude of the body’s displacement and on individual structural patterns.
The ankle strategy is most effective for small COG movements: the body acts
like a rigid mass and rotates about the ankle joints. This is possible by contracting
the ankle, thigh and lower trunk muscles.
The hip strategy, in contrast, is mostly used for large COG movements: the
body sways, moving the hips forward and backward with little ankle movement.
This generates horizontal reaction forces against the support surface opposite to
the direction of hip movement. The stepping strategy operates in order to avoid a
fall when the destabilizing force shifts the COG beyond the limits of stability
(Fig. 18.2) [1, 2].
S. Barozzi • F. Di Berardino
B. Monti
Private ENT Center “Otorinolaringoiatri Associati”,
Corso Stati Uniti 39, 10129 Turin, Italy
D.C. Alpini (*)
Milan, Italy

186 S. Barozzi et al.
Subject standing in Subject standing Subject standing on

vertical position with with flexed knees hips with lower
lower limbs in exten- limbs in extension
sion
Fig. 18.1 Position of centre of gravity in different standing postures
Ankle Hip
strategy strategy
Fig. 18.2 Different strategies to

counteract displacements of COG
18 Dynamic Posturography 187
Fig. 18.3 The Equitest system
18.1 Equitest: Description of the System
The Equitest system (NeuroCom International, Inc; Clackamas, Oregon) [3, 4] is a

dynamic posturography device which allows different movements of the support
surface and different conditions of integration of sensory inputs (Fig. 18.3).
The Equitest system consists of:
• A platform provided with pressure-sensitive strain gauges located in each quad-
rant. It can translate horizontally forward or backward and rotate about an axis
colinear with the ankle joint.
• A movable visual surface which encloses the patient’s visual surrounding and
rotates about an axis colinear with the ankle joint.
• Computer, monitor and printer which analyse, visualize and print data. The
Equitest standard protocol consists of two tests: (1) the sensory organization test
(SOT) and (2) the motor control test (MCT).
Fig. 18.4 The sensory

organization test
18.1.1 Sensory Organization Test
The SOT assesses the ability of a subject to use visual, vestibular or somatosensory
information to maintain upright stance under different sensory conditions [5, 6]. Tests
conditions are meant to isolate the function of each equilibrium subsystem by reduc-
ing the contribution of others or by presenting conflicting sensory inputs. Thus, during
the test, the platform and the visual surrounding are fixed or rotated proportionally to
any forward or backward sway of the subject (sway-referenced support and sway-
referenced visual surrounding) according to the following six combinations (Fig. 18.4):
1. Normal vision (fixed support)
2. Absent vision (fixed support)
3. Sway-referenced vision (fixed support)
Equilibrium score
100
75
50
25
NN NN
SS SS
Fall
1 2 3 4 5 6 Composite
Sensory conditions 84
Fig. 18.5 The composite score
4. Normal vision (sway-referenced support)

5. Absent vision (sway-referenced support)
6. Sway-referenced vision (sway-referenced support)
Information from a sense subjected to sway referencing suggests that the
orientation of the body’s COG relative to gravity is not changing when in fact it is.
Normally, individuals ignore a sway-referenced sensory input and maintain balance
by using other sensory inputs.
In addition to sway referencing, eyes-closed conditions are used to further isolate
the somatosensory and vestibular systems. The original test scheme does not reduce
or confound the contribution of the vestibular system. Head extension may also be
useful because it places the utricular otolith organs in a disadvantageous position
[7, 8]. Head extension also enhances cervical proprioceptive input; therefore, it could
be favourably employed in testing balance of whiplash-injured patients. To highlight
the importance of dynamic posturography to detect clinical equilibrium disturbances,
Fitzpatrick et al. [9] in a study on perturbed stance, showed that feedback control
alone does not allow stable balancing with large disturbances. In the same way, Horak
et al. [10] in 2002 observed that disturbance compensation, which is incomplete (only
partial) with small disturbances, increases with increasing stimulus magnitude.
A computerized system evaluates COG sways and calculates, for each test, the
equilibrium score, comparing the patient’s maximum anterior to posterior COG
displacement to the theoretical maximum displacement of 12.5°.
The Equitest analysis programme also calculates:
• The composite score, the average of all conditions’ scores (Fig. 18.5)
• Sensory analysis, which allows identification of a sensory dysfunction and/or an
abnormal sensory preference by calculating the ratios of different sensory
conditions (Fig. 18.6)
Fig. 18.6 The sensory Sensory analysis

analysis 100
75
50
25
0
SOM VIS VEST PREF
Fig. 18.7 The strategy Sensory analysis

analysis (ankle dominant) 100
Hip dominat
75
50
25
Ankle dominat
Fall
Hlp 25 50 75 Ank
• The strategy of movement adopted to maintain upright stance (ankle strategy, hip
strategy) (Fig. 18.7)
• The COG alignment (Fig. 18.8)
Fig. 18.8 The COG

alignment COG alignment
18.1.2 Motor Control Test
The MCT studies automatic postural responses to unexpected movements of the

base of support: small, medium and large backward translations; small, medium and
large forward translations. Each trial is analysed in terms of latency, amplitude and
symmetry of response. When the support surface is unexpectedly translated forward
or backward, the body initially remains stationary and becomes offset relative to the
base of support. The stiffness of ankle joints initially resists to the sway but is
insufficient to stabilize the COG sway.
In backward translations, when the ankle strategy is used to counteract the
forward displacement, a sequential activation of distal to proximal extensor muscles
is adopted (gastrocnemius, hamstrings, paraspinal muscles). These muscle
activations help to stabilize knee and hip joints so that the body moves as a coordi-
nated unit about the ankle joint [11].
When the hip strategy is used, we observe an activation of the flexor
muscles of the hip joint (quadriceps and abdominals) that moves the body
backward [12].
In forward translations, when the ankle strategy is used, we assist with a
sequential activation of distal to proximal flexor muscles (tibialis anterior, quadri-
ceps and abdominals).
In the hip strategy, the hip joint moves forward to activate paraspinal muscles and
hamstrings. In the MCT the platform is also tilted abruptly up and down to evaluate
adaptation to disruptive balance forces [13].
Patient: P. File: 930107A.EQT

Age: Referred by: Date: 01 Mar 1993
ID: Sway–Referenced Gain: 1.00 Operator ID: Time: 10:11
Weight symmetry Weight symmetry

Backward translations Forward translations
Left Right Left Right
S S
M M
L L
0 100 200 0 100 200

Latency (msec) Latency (msec)
Backward translations Forward translations
200 200
160 160
120 120
2 4 4 4 2 4 4 4
80 80
M L M L M L M L
Left Right Left Right
Amplitude scaling Amplitude scaling

25 ∗ = Left 25
= Right
20 20
15 15
10 10
∗
∗
5 5 ∗
∗ ∗
0 0
S M L S M L
Adaptation – Toes UP Adaptation – Toes Down

200 200
150 150
100 100
50 50
0 0
1 2 3 4 5 1 2 3 4 5
Fig. 18.9 The motor control test
Toes-up rotations of the support surface stimulate proprioceptors in the gastroc-

nemius muscles of both legs and elicit muscle forces which tend to destabilize pos-
ture [14, 15]. The adaptation test assesses the patient’s ability to ignore these
disruptive somatosensory inputs within five trials (Fig. 18.9).
18.2 Dynamic Posturography in Whiplash Injuries
The Equitest is a modern device which provides an objective assessment of

balance function in its entirety. With the composite score we have an individual
global equilibrium measure which can be compared to the average score of clini-
cally normal individuals of the same age.
Several studies made in the normal population confirmed the confidence and the
repeatability of computerized dynamic posturography results.
Many patients with “whiplash syndrome” experience unrelenting neck stiffness
and pain. This abnormal muscular tension is postulated to be causally related to a
central disorder of postural control, which has evolved secondary to injury of the
inner ear labyrinthine structures.
Moving platform posturography was used by Chester [16] to demonstrate the
presence or absence of a static or dynamic equilibrium disorder in 48 patients who
had experienced the oscillation forces induced by a rear-end automobile collision.
Other vestibular tests were used to document dysfunction of the semicircular canals
and the otolith structures. A high percentage of patients were found to have faulty
inner ear functioning, leading to inefficient muscular control of balance and erect
posture. Active perilymph fistulas were identified at surgery in seven patients.
Kogler et al. [17] investigated a total of 32 healthy subjects (16 men, 16 women,
age range 21–58 years), and ten patients age range 27–62 years (mean 44 years)
with neck problems and associated balance problems since a whiplash injury were
tested for postural control using the Equitest. The normal subjects were initially
split into four-age groups in order to estimate the effects of age on performance.
The postural stability was evaluated for dependence of support surface conditions
(stable or sway-referenced), visual input (eyes open or closed) and head position
(neutral, left rotated, right rotated, extended backwards or flexed forward). As
expected, visual cues as well as stable support surface improve postural stability
(p < 0.001). Postural stability is statistically different in the head-extended-backward
condition compared with the other four head positions (p < 0.001 in all cases) in
both patients and controls. Eliminating this test condition from the analysis, only a
slight (p < 0.05) difference between head forwards and head turned left remained.
This pattern of results remained if the normal subjects were only split into two age
groups instead of four. Finally, the patient group exhibited significantly lower pos-
tural performance than all the groups of normal subjects (p < 0.01), but none of the
normal groups differed significantly from each other. It is concluded that the pos-
tural control system is significantly challenged in the head-extended-backward con-
dition in both normal subjects and patients with previous whiplash injury and
persistent neck problems. The patient group differed statistically from all groups of
normal subjects. This suggests that neck problems impair postural control and that
the head-extended position is a more challenging task for the postural system to
adapt to.
Our experience in evaluating whiplash injuries has showed that in the SOT the
composite score can separate, in a confident manner, normal subjects at a conven-
tional neurotologic evaluation from pathological ones. The only discordance was
given by benign positional vertigo results which can be normal at SOT.
The opportunity to have available, objective and repeatable data is important in

medical-legal cases following whiplash injuries [18].
For this purpose computerized dynamic posturography can detect patients
who exaggerate symptoms of unsteadiness when test results are physiologically
inconsistent. In our experience, in case of deliberate exaggeration of symptoms, we
found one or more of the following inconsistent patterns:
1. Composite scores lower than 42 % in subjects who do not have ataxia and
ambulate without the use of balance aids.
2. Better performances under more difficult conditions (4–5–6) then under easier
ones (1–2–3).
3. Declining performances during successive trials, with a percentage of equilib-
rium in the first trial at least two standard deviations greater than the third.
4. Sinusoidal sway traces of COG.
5. Dispersion of the x–y plots of the initial COG alignment.
6. Sudden falls after periods of relative stability in the SOT.
7. Abnormal adaptation in toes-up and toes-down rotation. In our experience,
the 70 % of patients with cervical distortional trauma and with an abnormal
composite score and consistent test show vestibular dysfunction patterns on SOT
sensory analysis (the sensory ratio of conditions 5/1 is abnormal).
With somatosensory and visual inputs misleading and unavailable, such as in
condition 5, the upright position is allowed by otolith vestibular function which
controls the extensor antigravity muscles. Therefore, vestibular inputs assessed by
sensory analysis are prevalently from the otolith rather than from the canal organs.
For this reason in patients with peripheral vestibular disorders, Equitest results do
not always agree with caloric tests.
So, the abnormal vestibular function found in most patients with cervical trauma
can be explained by a deficit in the extensor antigravity muscles [19].
The motor control strategy most commonly observed in sequences of whiplash
injuries is the ankle strategy. This is evident in the strategy analysis where points
fall along a nearly vertical line on the right of the plot. This finding means that
patients are abnormally dependent on ankle movements even when the amplitude of
sway approaches the limits of stability.
In patients who underwent whiplash injuries, trauma directed to the cervical
spine usually reverberates along the whole column causing a hypofunction of the
erector muscles and a prevalence of the flexors which moves forward the body’s COG.
In order to resist the tendency of falling forward and to move the COG inside the
base of support, some corrective postural arrangements are used: forward trunk
flexion on the hip with consequent hip stiffness or flexion on the knees.
The choice of a strategy for balancing COG movements depends on personal
past experiences, on the individual history of previous accidents and pre-existent
muscle and joint impairments.
Therefore, although the ankle strategy is the most common pattern in cervical trau-
mas, this does not mean that it must be found in all patients with whiplash injuries.
In interpreting Equitest results, the strategy analysis can influence the choice of
rehabilitative treatment; in cases of prevailing ankle strategy, we adopt exercises
aimed at potentiating the extensor muscles and only afterwards exercises with the
purpose of recovering hip mobility.
In MCT the evaluation of latency offers interesting considerations: latencies
within normal ranges are observed either in forward or in backward translations
only in a limited number of patients with whiplash injuries. In our experience 86 %
of patients have abnormal latencies either in forward (10 %) or in backward transla-
tions (12 %) or in both (64 %). Response-strength scores and weight symmetry have
always been normal. In whiplash injuries abnormal latencies can be explained as
disorders in the afferent somatosensory pathways.
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The Cervico-Cephalic Interaction
19
D.C. Alpini, V. Mattei, D. Riva, and F. Di Berardino
19.1 Introduction
While the first function of posture is an antigravity function, the second one is to
provide an interface with the external world for perception and action. For this
reason, body posture is built up by a set of assembled segments with own mass that
are linked together by flexible joints controlled by the neuromuscular system.
Posture based on the superimposed segments (the head, the trunk and legs) is under
the specific automatic central and peripheral control preserving the specific
orientation of each segment with respect to gravity and/or to the adjacent segment.
The central organization of posture involves interactions between external forces,
the mechanical properties of the body and the neuromuscular forces.
Head stabilization appears to be a necessary motor control [1] in order to provide
a stable orientation platform (regarding both gravity and environment landmarks)
necessary for an adequate progression of body movement. Input from different
systems are essential to control posture and head stabilization and it has been
postulated [2] that high motor and sensory mechanism are necessary both for
simplest conditions like standing (posture control) [3] and walking (head control).
D.C. Alpini (*) • V. Mattei

ENT-Otoneurology Service, IRCCS “Don Carlo C. Gnocchi” Foundation,
Milan, Italy
D. Riva
International Society of Proprioception and Posture, via Valgioie 87,
10146 Torino, Italy
F. Di Berardino
Milan, Italy

Adequate posture and head controls are specific tasks of the vestibular system
[4], and they are particularly important in daily activities. Body is not a rigid block
but a flexible system formed by multiple segments tied together by the muscles sur-
rounding the joints. When a movement is performed by a standing subject, like
walking, the geometry of the body is changed. Dynamic posture, in fact, can be
considered as superimposed modules from feet to the head, each linked to the next
by a set of muscles which have their own specific central and peripheral regulation
serving to maintain the module reference position. The reference position of each
the modules can be regulated independently from that of the others. Dysfunction of
cervical receptors in neck disorders has been shown to lead to disturbances in pos-
tural stability, causing a disruption of the intricate coordination between eye, neck
and trunk movements. These changes in cervico-cephalic coordination may under-
lie clinical symptoms reported by people with WAD that involve changes in func-
tion during walking [5].
The aim of the chapter is to describe specific instrumental tests able to investi-
gate alteration of cervico-cephalic control provoked by whiplash.
19.2 CranioCorpoGraphy (CCG)
Head destabilization seems to be the specific target to investigate equilibrium dis-

turbances in whiplash patients. Since 1968, CranioCorpoGraphy (CCG) has been
used as a simple procedure to evaluate head-trunk stabilization in vestibular disor-
ders [6]. It has proved to be one of the most efficient, quick, objective and quantita-
tive tests for screening equilibrium function for nearly 20 years, and the West
German Labour Security Surveillance Board introduced it for occupational medi-
cal ability testing in 1983. CCG records light tracings from light bulbs on the
forehead, the occiput and both shoulders through a camera mounted from above
(Fig. 19.1).
The recording is displayed on film (Fig. 19.1b) from an instant camera fixed
above the head of the patient and directed towards a mirror on the ceiling. The results
are radar-like images, and the investigator evaluates a complete movement pattern
during stepping by visually inspecting the craniocorpogram. This enables the clini-
cian to differentiate between vertigo of central and of peripheral origin [7, 8].
CranioCorpoGraphy (CCG) has been successively digitalized (dCCG) on the
basis of the optoelectronic technology [9]. Digital CranioCorpoGraphy (dCCG) is a
non-invasive assessment based on a 50 Hz CCD camera for acquiring the position
of four markers placed on the subject who walks on the spot (Fukuda Stepping test)
(Fig. 19.2).
A digital stepping analyzer (DSA.) recognizes these markers and identifies their
2D positions in the horizontal plane. These rough data are then transferred to a
workstation through a universal asynchronous receiver transmitter (UART) for pro-
cessing and following elaborations. The UART allows a sampling rate of 25 Hz, and
so it fixes the maximum sampling rate of the whole system [9].
The output is a report that gives both analogue and quantitative information. The
subject performs the test blindfolded in a semi-darkened and sound-proofed room
19 The Cervico-Cephalic Interaction 199
that removes audio-visual orientation landmarks. Subjects are asked to walk on the
spot at their preferred speed for at least 30 s. Claussen and Claussen [7] used a
metronome in his experiments, but in our experiment the subjects walked at their
preferred speed to avoid the sound of a metronome distracting them. dCCG gives
qualitative information on the pattern of absolute movement and analyses the
following parameters for each marker and for the coupled head and shoulder (trunk)
markers:
Convex mirror
Camera
Rotor
Miners helmet
with head lamps
Eye mask
Shoulder lamp
Radar image like CGP
Fig. 19.1 A schematic representation of CGP (craniocorpography). Subjects walk on place in a

dark room, and movements of the light bulbs placed on the head (helmet) and shoulder impress the
film in an instant Polaroid camera in order to obtain four light traces on a black imagine
• Total distance: total distance (in cm) traced by the marker during body
movement.
• Speed: mean marker global speed (cm/s).
• Lateral speed: mean marker lateral component speed (cm/s).
• Longitudinal speed: mean marker longitudinal component.
• Global speed (cm/s).
• Head rotation: represents the absolute difference of head rotation in the transver-
sal plane from the beginning to the end of the test.
• Shoulder rotation: is the absolute difference of trunk rotation from the beginning
to the end of the test.
• Spin body: it shows the relative position of the head with respect to the trunk
during the stepping test.
• Index of coordination (%): because marker movement is composed of longitudi-
nal (body forward projection) and lateral (body sway) components, it compares
the two components to calculate lateral dispersion of body movement during
forward progression.
Due to the complexity of the data analysed for each marker, a coefficient of per-
formance (CP) was calculated to simplify the cut-off between normal and patho-
logical tests. CP clearly identified an abnormal stepping pattern.
Fig. 19.2 Two passive reflective markers (front and rear) are set at the extremities of a stick
attached to a worker’s hardhat, while two markers (left and right) are attached on rigid shoulder
supports
By means of dCCG, Alpini et al. [10] investigated 25 healthy subjects and 33

WAD’s patients. Whiplash patients were classified as chronic (more than 6 months
after injury) and recent (less than 6 months after injury). Clear differences
between healthy subjects and patients were seen and three different patterns were
detected:
• Pattern A: patients appeared similar to normals but quantitative analysis showed
significant differences with paradoxical head over-stabilization (collar-effect).
• Pattern B: with decreased head stability.
• Pattern C: with decreased head stabilization and reduced displacements of the
body.
Whiplash patients presented also different abnormal findings with respect to the
different parameters considered, but all of those with pattern B or C showed abnormal
CP, that to say whiplash patients presented a specific abnormality in head-to-trunk
stabilization. Head destabilization following whiplash may be correlated to a central
failure of head anticipatory stabilization. Anticipatory postural adjustments mean
that the onset of postural change occurred before the onset of the postural disturbance
due to the movement. Thus, a feedforward postural control is associated with move-
ment control, which prevents the posture and equilibrium disturbances associated
with movement performance from taking place. From these data, it seems that senso-
rimotor mechanisms progressively lose the ability to maintain head posture during
movement with a progressive alteration of movement pattern of the whole body the
longer the interval after trauma. Thus, while pain and neck stiffness are more frequent
in the early period from trauma, complex disorganization of dynamic equilibrium

seem to be a more significant feature later. Complete pattern disruption was evident
in patients with pattern C in which head velocity was increased, rotation of the shoul-
der and body torsion increased and dynamic control of body centre of mass lacking,
which lead to a nonprogressive or sometimes a backward stepping pattern.
Decreasing body forward progression may also be due to direct involvement of
thoracic and cervical muscle proprioceptive disturbance. Only in patients with a
‘normal’ stepping pattern (A) did the complex evaluation of stepping performance
indicate that the specific locomotor task was not disturbed. Thus, the CP is consis-
tent with and can indicate normality of stepping control.
Different stepping patterns in different subjects after similar injuries may be
explained by the intermodular model of postural control that may be controlled both
in a bottom-up and in a top-down manner according to the task and the environment.
In this way, whiplash could lead to significant alterations of dynamic postural con-
trol in those subjects preferentially organized with a top-down posture control.
In order to estimate the effects of cervical proprioception disturbance in WAD
group, only ‘chronic’ patients, with a trauma which occurred more than 6 months
before examination and still suffering neck pain and dizziness, were considered. All
the subjects, with eyes closed, walked on place on rigid surface (RIG) and on foam
(FOAM). In RIG test, head stabilization is depending on vestibular and propriocep-
tive cues, while in FOAM test, improved vestibular control of head stabilization is
required. Both NORM and WAD adopted a personal frequency of steps; the dura-
tion of test depends on the cadence of the subject considered since almost 60 steps
and 35 s were required. An optoelectronic system ELite (BTS Bioengineering
S.p.a.) (sample rate 25 Hz) [11] composed of two CCD cameras mounting wide-
angle objectives (C-Mount ¼″ with 2.8 mm focal length) was used. The two cam-
eras captured the movement of six passive markers placed on the subject (three
(front, rear, head) were fixed on an helmet referring to the head and three (left, right,
shoulder) were attached on two rigid shoulder supports defining the trunk)
(Fig. 19.3).
Cameras acquired the movement of the subject in the whole reference volume
that is about 1.5 m3 from a close range. The rough 3D data were filtered with an
adaptative low-pass filter (Butterworth – maximum cut-off frequency: 5 Hz); then
some parameters were computed, extrapolated from those used in the 2D analysis
with some improvements and innovation. The following parameters were
calculated:
• Global displacement [cm]: geometrical distance from the starting and the ending
position of the rigid body.
• Speed [cm/s]: ratio between the path (sum of the geometrical distances between
the positions assumed by the rigid body frame by frame) and the duration of the
test.
• Rotation [degrees]: rotation angle of the rigid body in the horizontal plane, com-
puted using ZYX Eulerian convention.
• Spin Body: sum of the of rotation angles of head and trunk in the horizontal
plane.
Fig. 19.3 Six markers

placed on the subjects: 1 1
mFront, 2 mRear, 3 mHead,
4 mLeft, 5 mRight, and 3
6 mShoulder. 1, 2 and 3 are
fixed on a rigid helmet
referring to the head, while
6 4 2
the others are attached on two
rigid shoulder supports
defining the trunk
• Disharmony: it represents the capability of the subject to keep the same stepping
frequency during the test. High values of this parameter indicate an incapability
to keep the same pace during the test.
• Steps per minute: number of steps made in the trial normalized with the duration
of the test in minutes. The number of steps was computed starting from the lat-
eral path. In particular the change of sign of the first derivative of this variable
was assumed to be a step. So the sum of all these changes normalized to the
duration of the trial corresponds to the step per minute parameter.
• Index of coordination (IOC): ratio between an ideal path and the global path.
• Instability: it is the capability of the subject to maintain the same position after
the double step. High values indicate the incapability to stay on the place during
the test. In particular, instability is the ratio between the ideal path (previously
computed) projected onto the two components lateral and longitudinal and the
number of barycenters of cluster of data.
• Coefficient of performance (CP) was implemented (see Eq. 19.1). It is defined as
the normalized sum of the statistically meaningful parameters (N).
 p 
Log  k  j
N
 0.05   Parameterk  (19.1)
CP = ∑  
K =1 PTOT  ParameterHEALTHY 
All the parameters, with the only exception of rotations and trunk lateral dis-
placement, show higher values in WAD than in NORM (Fig. 19.4).
Closed eyes foam

Median: Box: 25 %, 75 %: Whishker: Min, Max
12
10
0
H Lat instability T Lat instability H Lon instability T Lon instability
Healthy
Whiplash
Fig. 19.4 Head and trunk lateral/longitudinal instability: comparison between healthy subjects
and whiplash people. Data are expressed as median, 25th and 75th percentiles b( ox) and maximum
and minimum values (whisker). All the differences are statistically meaningful
CP for WAD people

4
3.5
3
2.5
CP
2
1.5
1
0.5
0
Fig. 19.5 Coefficient of performance for whiplash people: each subject presents higher value
than normalcy
All the parameters that presented significant differences were used to calculate
CP. Figure 19.5, shows that CP increases 57 % in WAD people with respect to
NORM (the median values of the normalcy is about 1).
Stepping on a foam requires optimization of vestibular control. Generally speak-
ing, findings show that WAD are disturbed in keeping the segment head to trunk
during locomotion as a rigid body. While in healthy people sensorimotor control is

as efficient despite surface conditions, in whiplash people vestibular system seems
no more able to provide adequate head control if it is not sufficiently supplied by
podalic cues.
The hypothesis of rigid bodies is also useful to lead the analysis on the three
anatomical components of some of the described parameters since it allows to
define the subject reference system. As a matter of fact, the CP is able to well char-
acterize the two groups, with high values of CP in WAD (Fig. 19.5), making feasible
a possible clinical application of this tool.
WAD present lower (not statistically significant) rotations due to their lower step
frequency and to the duration of the test that is shorter than healthy people and so it
is probably stopped before the beginning of rotation.
dCCG (2D and 3D) have been performed by means of prototypes. A CCG
commercial equipment is CMS 70P (Zebris, Tubingen). It consists of a measur-
ing sensor with integrated revaluation electronics and stand, a PC plug-in card.
The measuring procedure is based on the exact determination of the 3D posi-
tion of small ultrasound transmitters as markers, by measurement of the sound
pulse time. The measuring system operates up to distance of 2 m. Markers are
attached in a standard manner by means of adhesive patches to the hip, knee,
ankle and ball of the foot on both sides of the body. To determine the gait
phases, thin foot contact switches are stuck to the heel and the ball of the foot.
The left and the right side of the body are measured in succession. After the
interactive selection of the time segments to be analysed, a report is automati-
cally prepared. Here, angles of the joints, the foot rotation and the lateral move-
ments of the extremities are presented as time-dependent curves and as
maximum values. The individual gait phases, the step length, the cadence and
the average speed are evaluated. Information about instabilities is obtained
from the averaged and normalized curves of all individual steps and their stan-
dard deviation.
Experiments performed with dCCG suggest that the most specific parameter able
to discriminate between normal and pathological cervico-cephalic control is the
ratio between head and trunk displacements. It is so possible to detect directly head
and trunk sagittal (Y) and lateral (X) movements using a commercial equipment
(Delos, Turin, Italy) that uses two accelerometers 2D sensitive [12], respectively,
fixed to the occiput and to the sternum (Fig. 19.6).
Delos equipment records 20″ body segments movements each test. The follow-
ing parameters are calculated:
• Total displacement of each segment (degrees) in X and Y plane.
• Bi-dimensional total displacements of the body segment. In this way a
stabilogram-like imagine can be obtained (Fig. 19.7).
• X and Y velocities (degrees/s) for each segment.
• Head-to-trunk stability index (ratio between X or Y head and trunk displace-
ment). A ratio <1 indicates stabilization of the head with respect of the trunk.
Normal values range from 0.6 to 0.8. Values around 1 are considered border line,
while ratio >1 are pathological.
Fig. 19.6 An accelerometer

is fixed on the head and the
other on the trunk in order to
record sagittal and lateral
displacements of the two
body segments
Two standard tests allow to investigate head-to-trunk stabilization:

• Head Stabilization Stance Test: evaluation of head-to-trunk stabilization during quiet
steady stance (H-STAN) with eyes open and closed on firm and foam surfaces
• Stepping Test (STEP): evaluation of skill to maintain head stable with respect to
the trunk during walking on place
19.2.1 H-STAN
Maintaining postural stability involves coordination of mechanical components of

the limbs, the trunk and the head and sensorimotor antigravitary network, and it
requires a correct perception either of the position of whole body with respect to the
environment or the reciprocal position of each body segment. In quiet stance body
segments are aligned along vertical axis, and they are theoretically stabilized one
with respect to the other (e.g. head with respect to the trunk) during body oscilla-
tions that occur along the ankles maintaining upright position (Fig. 19.8).
Fig. 19.7 Stabilogram-like images obtained during a standard five-conditions (eyes open and
closed on firm and foam surface, head retroflexion) posturographic test by means of trunk
accelerometer
In whiplash patients, this test is as frequently abnormal in eyes-closed condition

on foam as the trauma is recent, that to say that cervical muscles are not able to coun-
teract trunk sway in order to maintain body as a whole rigid inverted pendulum.
Head and trunk sway are represented as superimposed cones. In normals (left)
head cone is smaller than trunk cone and head-to-trunk ratio is less than 1, while in
a patient (right) the pattern is reversed.
19.2.2 STEP
Patients were requested to quietly walk on place in a quiet room in two different
conditions: eyes open and eyes closed.
Different findings have been noted regarding dynamic head stabilization during
walking on place. Human walking is a complex activity, and maintenance of equilib-
rium is a particularly challenging task for the human postural control system because
our centre of mass is located a considerable distance from the supporting surface and
for a major period of the walking cycle the body is supported by a single limb with
the centre of gravity (CG) passing outside the base of support. During locomotion,
alignment and respective balance control of each superimposed segment have to be
continuatively controlled in order to provide head stabilization (Fig. 19.9).
In chronic whiplash, patient’s abnormal head-to-trunk pattern in X and or Y plane
can be recorded with same frequency of the experimental data obtained by dCCG.
Fig. 19.8 H-STAN
30.2° Head 53.8°
velocity
degrees/s
37.8° Trunk 39.6°

velocity
degrees/s
Head-to-trunk Head-to-trunk
x plane ratio 0.8 x plane ratio 1.4
Fig. 19.9 As in Fig. 19.8 at

left a normal STEP test and at 284.6°
right a pathological tests with 308
Head
increased head sway with velocity
respect to the trunk degrees/s
322.5° 258
Trunk Head-to-trunk
velocity x plane ratio 1.2
Head-to-trunk
x plane ratio 0.8
19.3 Smooth Pursuit Neck Torsion Test (SPNT)
Whiplash produces a complex disturbance of sensorimotor control of oculomotion,

balance and locomotion, involving both peripheral and central processing of eye-
head-neck coordination [13].
In 1998 Tjell and Rosenhall [ 14] firstly described a specific oculomotor test,
named smooth pursuit neck torsion test (SPNTT). This test was shown to possess
such high sensitivity and specificity for chronic whiplash-associated disorders that
it was proposed as a diagnostic test. In 2005 Treleaven et al. [15] re-proposed this
oculographic test. Electrooculography (EOG) is used to measure and record eye
movement while following a moving target.
The procedure we use in our laboratory is similar to those described by Tjell
et al. [14] and Treleaven et al. [15]. The target consists of a light spot projected
into a TV screen through a visual angle of 30°. The target is electronically con -
trolled to provide a moving sinusoidal stimulus with a maximum velocity of 30°
per second and a frequency ranging from 0.2 to 0.4 Hz. Pairs of Ag/AgCl surface
electrodes are placed on the skin just lateral to the eyes bilaterally to record eye
movement via changes in the corneo-retinal potential. A ground electrode is
placed on the forehead. The signals are passed through a 70 Hz low-pass filter and
stored on an IBM-compatible PC that continually records the change in corneo-
retinal potential and eye position relative to the target during each test sequence
(in our Lab EOG equipment by Toennies, Germany). The data is stored for later
analysis. For each test the average velocity of the eye movements as they followed
the target is calculated by subtracting the corrective movements from the total
excursion of the gaze. A software program identifies and subtracts the corrective
saccades (when the eyes moved more than twice as fast as the target for at least
20 ms, this was registered as a saccade). The program then formulates the cor-
rected gain for each cycle. The signal is excluded when a blink is present, and in
case of severe disturbances in the EOG signal, the entire tracking from one side of
the screen to the other is excluded. Square waves and blinks (judged from recorded
examples of an actual blink from each subject) are disregarded from the analysis.
The mean gain (i.e. the ratio between the eye movements and of target) is the
measure used to define smooth pursuit movements. Hence, the gain had the value
of ‘1’ when no corrective saccades were registered throughout the entire
recording.
The smooth pursuit (SP) gain is calculated with the neck in a neutral position and
also with the neck in a torsioned position. The average gain for neutral (SP neutral)
and torsion to the left (SP left) and right (SP right) is calculated. The difference
between the gain in neutral and the average values in torsion equalled the smooth
pursuit neck torsion difference (SPNT- diff):
gain [ neutral] − ( gain [ left ] + gain [ right ]) / 2

The SPNT-diff thus equals 0 if the smooth pursuit eye movement’s performance
did not differ between the neutral and the rotated positions.
Tjell and Rosenhall reported that the sensitivity of the SPNTT test in the WAD
group with dizziness was 90 % and the specificity was 91 %. The sensitivity in the
WAD group without dizziness was 56 %. They concluded that SPNTT seemed to be
useful for diagnosing cervical dizziness, at least in patients with WAD having symp-
toms of dizziness, because it has a high sensitivity and specificity.
Treleaven et al., on one hand confirmed the high sensitivity of the test, on the
other, underlined that there was a risk of bias because eye movement analyses were
performed by manual methods.
Yu et al. in 2011[16], studying the neck torsion manoeuvre used in the smooth
pursuit neck torsion, have shown that there is an increased amplitude of sway when
measuring in the anterior-posterior direction following neck torsion in WAD com-
pared to healthy subjects. This cervical interference could be another bias to be
taken in account in the evaluation of SPNNT.
In our experience, the use of a standardized EOG equipment with rigorous cali-
bration procedures before each recording is enough to counteract ‘technical record-
ing bias’.
To avoid ‘cervical bias’ is necessary to slowly rotate the chair and to use a head
rest to avoid neck fatigue and head sway.
In our laboratory, we standardized SPPNT investigating two groups of chronic
WAD patients, one complaining of neck pain stiffness and one without dizziness.
In both WAD groups neck torsion reduced the SP gain (p < 0.001), and in control
patients with central and peripheral or in the healthy control subjects, it did not.
The sensitivity of the SPNT test in the WAD group with dizziness was 90 % and
the specificity was 91 %. The sensitivity in the WAD group without dizziness
was 56 %.
In our experience, SPNT test seems to be useful for diagnosing cervical dizzi-
ness, at least in patients with WAD having symptoms of dizziness. Our results in the
neck torsion positions are similar to those documented by Tjell and colleagues [14]
and Hildingson et al. [17] although the overall difference (SPNT) was slightly
smaller on average than that of Tjell and colleagues.
Our results add support to the validity of the SPNT test to detect physiological
impairments in patients following a whiplash injury. No associations were observed
between smooth pursuit eye movement recordings in the neutral seated position at
that time and symptoms. Furthermore, the results of the SPNT were not influenced
by medication or compensation status.
High sensitivity of the test is possibly a consequence of damaged cervical pro-
prioception, as suggested by the inventors of the test.
SPNT test suggests that the differences between the whiplash and control sub-
jects are most likely due to disturbances to the postural control system, specifically,
primary altered afferent input from the cervical spine. It could be argued that the
torsion manoeuvre could stress the vertebral artery, but this is quite impossible if the
movement of the neck is a pure and limited (45°) rotation without any degree of
extension or flexion. Furthermore, any reduced blood flow in the vertebral artery is
likely to be asymptomatic in neck torsion manoeuvres due to compensation by col-
lateral vessels [18].
Nevertheless concomitant pathology and secondary adaptive changes in brain-
stem mechanisms as a result of the altered central modulation of cervical afferent
input are possible, and future studies to determine the importance of these factors
following a whiplash injury are necessary [19, 20].
The underlying mechanisms of the deficits measured in the SPNT test appear
that both cervical proprioceptive and nocioceptive factors, as well as others, may
contribute to the eye movement disturbances found in patients with persistent
whiplash-associated disorders.
In conclusion, SPNTT is a simple and sensitive test even if the disturbances in
patients with persistent neck pain following a whiplash injury have to be considered
multifactorial and rigorous recording and torsion procedures are necessary [21].
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Neurotology in Whiplash Injuries:
Vestibulo-ocular Reflexes and Visuo- 20
vestibular Interaction
L.M. Odkvist, A. Cesarani, and F. Di Berardino
20.1 Introduction
Apart from the most serious neurological disturbances, otoneurological clinical fea-
tures are very important elements in cervical whiplash. Approximately 10 % of
patients [1] who have suffered with whiplash injury will develop otological symp-
toms such as tinnitus, hearing loss, dizziness and vertigo. Some of these are purely
subjective symptoms; nevertheless, for the majority there are specific tests that can
be undertaken. According to Claussen and Claussen [2], about 15–20 % of subjects
involved in a traffic accident develop the so-called late whiplash injury syndrome in
which the individual patterns of functional lesions may be documented through
appropriated neuro-otological tests.
Vertigo – which can be of different types – is one of the most common symptoms
if not the most frequent one. On the other hand, whiplash-associated hearing loss is
not frequent: Rowlands et al. [3] did not release any patients with otological lesion
in the acute phase following their whiplash injury. This suggests that caution should
be exercised when attributing these symptoms to such an injury. Before whiplash
injuries are admitted as an aetiological factor in the development of such symptoms,
other causes should be excluded.
L.M. Odkvist
Department of Otolaryngology, University Hospital, S-58185
Linkoping, Sweden
A. Cesarani • F. Di Berardino (*)
e-mail: antonio.cesarani@unimi.it; federica.diberardino@unimi.it

214 L.M. Odkvist et al.
20.2 Peripheral Whiplash-Associated Vestibular Involvement
For balancing, motor control and keeping visual objects steady on the retina, the
vestibular system and the interaction with the visual system are of paramount
importance. Balance is maintained via cooperation between the vestibular afferents,
proprioception, podalic pressure receptors and vision [4]. For diagnostics postural
tests are important, but the easiest and most accurate way to study the vestibular
system is recording of spontaneous and provoked eye movements and the interac-
tion with the visual system. Often the cause for vertigo can be unveiled with these
methods. For eye-movement recording, the most widely used methods are electro-
nystagmography (ENG) [5] and videonystagmography (VNG) [6].
Whiplash-associated vestibular symptoms are variable in relation to either the
type and intensity or the temporal course of clinical manifestations. These symp-
toms include positional vertigo, which can also last for 2 years [7, 8]; latent nystag-
mus which appeared in about 30 % of the patients either within or after a year
following the trauma [9]; and spontaneous nystagmus in more than 50 % of the
subjects, in most cases of positional type. In many subjects the positional nystag-
mus was direction-fixed, in others direction-changing, and the results of Dix-
Hallpike manoeuvre suggested the possibility of otolithic damage with cupulolithiasis
of the posterior semicircular canal [10]. We must also remember that latent nystag-
mus, pathological monolateral caloric test and anomalous rotatory test, even later
than a year after the trauma, may be observed in a great number of patients.
Despite clear symptoms, it is difficult to find objective standards to produce evi-
dence for the presence of the ailment in patients with WAD. However, Kelders et al.
[11] recently found that the gain of one of the ocular stabilization reflexes, the
cervico-ocular reflex (COR), was elevated in patients with whiplash injury com-
pared with an age-matched control group.
The COR acts in conjunction with the vestibulo-ocular reflex (VOR) and the
optokinetic reflex (OKR) to preserve stable vision on the retina during head motion.
It is elicited by rotation of the neck, thereby stimulating proprioceptive afferents
from deep neck muscles and joint capsule from C1 to C3 to the vestibular nucleus,
leading to eye movements that oppose the direction of the head movement [12].
The VOR can be subdivided into rotational and translational components induced
by stimulation of the semicircular canals and the otolithic organs, respectively.
When the head is turned, the VOR moves the eyes in the opposite direction, respond-
ing optimally to high frequencies. The OKR is stimulated by visual motion and uses
the relative velocity of the image on the peripheral retina to generate eye move-
ments in the same direction. OKR and COR reflexes respond best at low head
movement velocities. Gain values of the COR are increased over a broad range of
velocities (1.2–12.8°/s) in patients with whiplash injury, though the largest differ-
ence was found at lower velocities [13].
In healthy persons, COR gain can be modified after 10 min of concurrent visual
and cervical stimulation. In patients with absent vestibular function, COR gain is
also increased, as it is with age (older than 60 years). Meanwhile, in elderly persons,
the gains of the VOR and OKR are decreased.
20 Neurotology in Whiplash Injuries 215
20.3 Vestibulo-Oculomotor Reflex (VOR)
Examination of ocular movements in response to stimulation of the vestibular part of

the inner ear is important for evaluation of the state of the vestibular system in patients.
The vestibulo-ocular reflex (VOR) connects the sensory transducers, the hair cells in
the semicircular canals and the otolithic organs in the vestibular part of the labyrinth
with the extrinsic ocular muscles. Stimulation of the inner ears results in movements
of the eyes. With VOR, during head movements the visual target is always centred on
the fovea. Vestibular stimulation is achieved either by rotatory movements of the head
or, in the caloric test, thermal irrigation of the ear canal. The advantage of the caloric
test is that it tests each labyrinth separately. Caloric irrigation is, however, a crude and
unphysiological stimulus. The rotatory test, on the other hand, uses a more physiolog-
ical stimulus, however exciting both ears simultaneously.
A thermic stimulation of the labyrinth is usually achieved using water with a
temperature 7° above or below body temperature. The patient lies down with the
head elevated 30° from horizontal. The test is based on the fact that the calorie
stimulation induces a movement of the endolymph in the semicircular canals [14].
A nystagmus is elicited and calculated concerning different qualities of the reaction.
Sometimes the duration of the nystagmus response is recorded, but the most valid
parameter is the speed of the slow phase of the elicited nystagmus beats. The dura-
tion of the reaction is an uncertain measurement of the calorie response and can be
normal although a diminished calorie response may be present, which is unveiled
only by measuring the speed of the slow phase of the nystagmus beat.
Rotatory testing has been in use since the turn of the century. The main drawback
with the rotatory test is that the stimulation affects both labyrinths simultaneously.
The equipment for rotatory testing is usually expensive and complicated. One
advantage with the rotatory test is that the eye movement responses are not depen-
dent on the individual anatomical variations and the recordings can be performed on
subjects who do not tolerate caloric irrigation.
One additional advantage is that rotatory test provides a natural physiological
acceleration stimulus. Different stimulus patterns have been used in rotatory testing
– trapezoidal, triangular and damped sinusoidal. A vast amount of data has been
collected from rotatory testing using broad frequency swings (0.5–5 Hz) [14].
The autorotation test, an interesting VOR test, uses the equipment for ENG, but
the patient himself sinusoidally turns the head to the right and left rhythmically [15].
A calculation is made of the difference between the head movements and the eye
movements. The equipment is inexpensive and easy to handle, but the drawback is
that cervical influences cannot be avoided. Thus the test is not useful in cases of
cervical vertigo or whiplash injuries [16–18].
The head shaking test is a simple way of testing the vestibulo-oculomotor sys-
tem: The patient shakes his head with a frequency of 1–2 Hz for 10 s. Immediately
after stopping the movement, eye movements are observed under Frenzel glasses or
preferably recorded by ENG. A post-head shake nystagmus for several seconds
indicates that there is an asymmetry in the peripheral or central part of the vestibular
system [19].
The otolithic influence on VOR may be evaluated by eccentric rotatory testing

that can unveil unilateral or bilateral function loss in the otolithic organs. During the
rotation the subject experiences an illusion of tilt and in the darkness places a bias
light bar at an angle to true horizontal and even has a tilt of the eyeballs. This type
of investigation is still not fully validated [20, 21].
20.4 Vestibulo-Visual Interaction
The directioning of the eyes is a function of the cooperation of the vestibular

organs, neck proprioception and vision. In cases of conflict, the visual reflexes
override VOR at least in the low-frequency area. In high-frequency swings, the
ocular motion is driven mainly by VOR. The cerebellar flocculus and nodulus
mediate the interaction. Patients with cerebellar lesions may have a defunct
visual suppression ability. Some patients with brainstem lesions may have the
same functional defect. The neck proprioceptors also help maintain gaze direc-
tion during movements of the neck, body and towards visible targets. In some
cases of neck lesions, a simple turning of the head to the right or left may elicit
a nystagmus, which can be studied preferably with ENG. Cervical influence on
the vestibulo-oculomotor system may also be unveiled if the patient is sitting in
a swing chair, the head is held steady by the examiner and the eye movements are
observed while the chair with the patient is turned rhythmically clockwise and
counterclockwise.
20.5 Visual Suppression of VOR
The vestibulo-ocular reflex cancelling or visual suppression mechanism can be

tested during the caloric response in darkness when a lamp is lit for 10 s, allowing
ocular fixation. The induced eye-movement speed should decrease to 30 % of its
value in darkness (Fig. 20.1). The visual suppression test becomes even more
Cal. 30°C right Visual suppression S.L.
gain=0,6
(norm. 0–0.3)
10°
1 sec. 14°/s 8°/s
Fig. 20.1 Pathological visual suppression in a patient with a brainstem lesion. Fixation nystag-
mus is still present at different velocity
sensitive if it is performed in the rotatory chair with the instruction to the patient to
fixate on a target by moving with the chair [22, 23] (Fig. 20.2).
20.6 COR Recordings
By passively rotating the body while fixating the subject’s head (trunk-to-head rota-
tion), isolated COR responses were recorded in the absence of visual or vestibular
input. The subject’s head was fixed in space by means of a custom-made bite board,
and the trunk was fixed to the chair by a double-belt system at shoulder level.
A cervical range-of-motion device was used to demonstrate that the head was suffi-
ciently stabilized in space, with negligible head movement induced by chair motion.
Nacci et al. [24] evaluated subacute whiplash-associated labyrinth involvement.
They submitted a group of patients within 15 days of the trauma to the following
tests: liminal tone audiometry, investigation for spontaneous nystagmus (positional
and positioning, with or without Frenzel glasses) and the head-shaking test (HST).
In addition, all subjects underwent a vestibular bithermal caloric balance test
according to Fitzgerald-Hallpike and videonystagmographic investigation. Analysis
of videonystagmographic investigations showed that it is possible to find both
peripheral (non-compensated/compensated labyrinth deficit and PPV) and central
(vertical nystagmus) vestibulopathy. Data collected in this study confirm that PPV
is possible in cervical whiplash trauma as well, even though it is more frequent in
cases of minor head injury (3 % vs. 10 %).
MacNab [25] attributes tinnitus, hypoacusia and pathological nystagmus follow-
ing an indirect injury in the cervical spine to a spasm in vertebral arteries. According
the author, the majority of neuro-otological injuries seen after an episode of whip-
lash are probably attributable to ischaemic or haemorrhagic events in the labyrinth
Fig. 20.2 Visual suppression test in the rotatory chair. Head movements are recorded with accel-
erometer on the bite-board. Eye movements are recorded with electronystagmography. The
instruction is to fixate on the dot on the screen moving by the chair. Thus the target is always right
in front of the eyes

b
membrane (peripheral vestibulopathy, tinnitus, sensorineural hypoacusia) or to con-

cussion and/or brainstem stretching (central vestibulopathy, tinnitus).
COR gain values in patients with WAD are significantly increased compared with
those in healthy controls [26]. An age-related increase was not seen in patients,
which could indicate that the whiplash injury cancels out this age-related effect
[27– 29]. In contrast to what was found in healthy controls, no synergy was found
between COR and VOR in the patient group. Furthermore, no correlation was found
between the remaining eye reflex combinations in patients and in controls. The
increase in COR gain in elderly patients might be an adjustment for the decline in
VOR gain [30]. Rijkaart et al. [28] showed that the COR is able to adapt after only
10 min of incongruent simultaneous visual and cervical stimulation. A decrease in
VOR gain might have been responsible for an increase in COR gain in our whiplash
patients, as seen in elderly subjects and in those with labyrinthine defects. However,
a higher COR gain could also be the cause of a decline in VOR gain. Earlier experi-
ments showed that the VOR gain could be adapted in 1 h by noncorresponding ves-
tibular and visual information. Contrary to the latter theory, the COR gain was
elevated with no decline in the VOR gain in WAD patients. Three hypotheses [28, 30]
can provide an explanation for this lack of synergy in patients with whiplash injury:
First, it may be that decreased mobility of the neck leads to alteration in proprio-
ception of the neck, which in turn results in an augmented gain of the COR without
any problems in the VOR pathway.
Second, it may be that adaptation of the VOR requires sufficient head motion
and, because of impaired neck motion, the patient has too little adaptive input for
the VOR to induce a negative adaptation in VOR gain. It is known that the VOR
responds best at high velocities, whereas the COR is most responsive at low fre-
quencies. This could explain the lack of decrease in VOR gain.
Third, it may be that there is a disorganization in the process of VOR plasticity
because of microtrauma in the VOR pathway, such as in the flocculonodular area of the
cerebellum. The latter hypothesis will be subject to more research in the near future
when we perform VOR adaptation experiments in patients with whiplash injury.
It can be speculated to what degree abnormalities in COR gain are responsible
for the reported signs and symptoms. Although the correlation between them is
striking, correlation does not prove causation. However, the results might explain
some symptoms. Improperly tuned VOR and COR may lead to symptoms such as
dizziness and to visual problems such as reading impairment. The absence of syn-
ergy between COR and VOR combined with head and neck pain may induce symp-
toms of fatigue.
20.7 Peripheral Whiplash-Associated Auditory Involvement
Hearing loss is frequent in general population, but it is not particularly frequent in

whiplash-associated disorders. Tjell et al. [31] investigated 153 ambulatory WAD
patients by means of pure-tone audiometry. Their audiograms were compared with
ISO standards. Fourteen percent of patients with WAD had a hearing impairment
exceeding the 90th percentile of the ISO standards. However, in most cases the
hearing was not associated with whiplash injury. A subgroup (33 patients) – with
normal hearing or slight hearing impairment according to the audiogram – was
selected from the total group of patients with WAD. The 33 selected patients and 33
matched controls were tested with the speech-in-noise test (SRN test). However,
40 % of this subgroup of patients with WAD reported hearing problems. As many
as 30 % of the patients with WAD had an abnormal SRN test result, as against 5 %
of the controls. Significant relations were found between the SRN test and self-
assessed hearing loss.
Thus the speech-in-noise test (SRN test) seems the most specific test to docu-
ment hearing involvement in WAD.
The specific involvement of the peripheral auditory system is confirmed by Segal
et al. [32] that conducted a retrospective review of clinical, pure tone and speech
audiometric findings. The first evaluation was obtained within 3 months and the
follow-up ones between 6 and 12 months after injury. Eighty-three patients (166
ears) reported hearing impairment after blunt neck trauma: Twenty of the 166 ears
(12 %) had normal hearing and 137 ears (81.3 %) showed an acoustic trauma-like
hearing impairment. Eight ears (4.8 %) had a hearing loss of at least 30 dB in the
speech frequencies (500–2,000 Hz), and two ears (1.2 %) had additional impair-
ment in the higher frequencies. Only one ear (0.8 %) had a conductive hearing loss.
No speech discrimination score was poorer than 80 %. Forty-six subjects (55.4 %)
reported tinnitus.
Whiplash-associated tinnitus was extensively investigated by Kreuzer et al.

[33] by means of demographic data, tinnitus-related clinical data, audiological
data, the Tinnitus Handicap Inventory, the Tinnitus Questionnaire, the Beck
Depression Inventory, various numeric tinnitus rating scales and the World
Health Organisation Quality (WHOQOL). The results indicate differences
between tinnitus patients with and without trauma at tinnitus onset: Patients suf-
fering from trauma-associated tinnitus suffer from a higher mental burden than
tinnitus patients presenting with phantom perceptions based on other or unknown
etiologic factors. This is especially the case for patients with whiplash and head
trauma. Patients with posttraumatic noise-related tinnitus experience more fre-
quently hyperacusis, were younger, had longer tinnitus duration and were more
frequently of male gender.
On the other hand, a benign cause of otological disorder, at least as acute onset,
has to be excluded as suggested by Ferrari [34] that investigated 86 whiplash
patients affected with earache, fullness in the ear, diminished hearing and tinnitus.
Out of 71 subjects reporting no acute onset (within 7 days of the collision that
caused their whiplash), 62 had little or no cerumen occlusion, but of eight subjects
reporting one or more of acute-onset earache, fullness in the ears, diminished hear-
ing and tinnitus, seven had complete cerumen occlusion in the affected ear. This
author underlines that his findings suggest high-grade cerumen occlusion frequently
occurs in the ear affected by acute auditory symptoms and that a number of acute-
onset auditory symptoms reported in whiplash patients may have a benign cause not
whiplash associated.
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Vestibular Evoked Potentials
in Relapsing Paroxysmal Positional 21
Vertigo
F. Di Berardino, D.C. Alpini, L. Pugnetti, V. Mattei,

and B. Franz
21.1 Introduction
Paroxysmal positioning vertigo (PPV) is a major cause of vertigo accounting for

14 % of all equilibrium disorders with an annual incidence of about 100 per 100,000
of population [1]. It starts suddenly and is usually first noticed in bed, when waking
from sleep. Any turn of the head seems to bring on violent but brief bursts of dizzi-
ness. Patients often describe the occurrence of vertigo with tilting of the head, look-
ing up or down, or rolling over in bed. It is not unusual for nausea and vomiting to
accompany the vertigo. Even if a spell is brief, a feeling of queasiness may last
several minutes or even hours, and those who suffer from this kind of vertigo are
distressed and incapacitated for several days severely impacting on social costs due
to lost working days. PPV is a common vestibular disorder leading to significant
morbidity, psychosocial impact, and medical costs. PPV accounted for 8 % of
individuals with moderate or severe dizziness/vertigo. Is commonly accepted that
PPV is due to displacement of otoconia and/or to vestibular macula/maculae lesion.
PPV is very common after whiplash head trauma, while it is very rare in cases
with a pure cervical involvement. In these cases, maybe through inner ear
F. Di Berardino (*)
Department of Clinical Sciences and Community Health, University of Milan,
Milan, Italy
e-mail: fdibe@fastwebnet.it
D.C. Alpini • L. Pugnetti • V. Mattei
ENT-Otoneurology Service, IRCCS “Don Carlo C. Gnocchi” Foundation, Milan, Italy
B. Franz
Department of Anatomy and Cell Biology, Tinnitus Research and Balance Clinic,
University of Melbourne, Wantirna, VIC, Australia

224 F. Di Berardino et al.
concussion or vertebral artery spasm, prolonged PPV, atypical PPV, or relapsing

PPV are the most observed forms [2].
Vestibular evoked myogenic potentials (VEMPs) are nowadays the specific test
to investigate vestibular maculae function, that is to say the site of origin of PPV.
They have been described [3, 4] as short-latency potentials from an active elec-
trode placed just below the inion in response to acoustic stimulation (the “inion
response”), probably generated by reflex changes in the electromyogram of poste-
rior neck muscles. Cody and Bickford [5] described the inion response [6] in sub-
jects suffering from different cochlear and vestibular syndromes and provided
further evidence to suggest that it depended on the activation of the saccular macula.
Those authors concluded that VEMP recording depended on the activation of a
specific reflex function called the vestibulocollic reflex (VCR), mediated by a path-
way consisting of the saccular macula, its primary neurons, vestibulospinal neurons
from the lateral vestibular nucleus, the medial vestibulospinal tract, and, finally, the
motor neurons of the spinal cord reaching neck muscles.
Recent studies showed that rarefaction clicks are preferred for evoking the sac-
cular response and that the sternocleidomastoid muscle (SCM) is the most advisable
recording site [7–9]. Healthy subjects produce a biphasic response from the SCM
characterized by a positive peak at a latency of some 13 ms (P1) from the stimulus
followed by a negative wave peaking some 10 ms later (N2). Abnormal results,
ranging from prolonged latencies to total absence of the response, disclose lesions
anywhere in the VCR pathway.
Vestibular evoked myogenic potentials (VEMPs) are commonly used to assess
the otolithic organ through a multineuron reflex test. A variant of VEMPs, the so-
called periocular VEMPs, in which potentials are derived from periocular muscles,
has been proposed as a specific test for utricolo-spinal reflexes [10, 11].
Franz et al. [12, 13] described a single neuron reflex test for the specific examina-
tion of the vestibular responses during sagittal and lateral tilts of the head (electro-
vestibulography, EVG). In this technique an extratympanic electrode is placed in the
tympanic recess for the recording of evoked potentials. Tilting the head in roll and
in pitch is employed to stimulate mainly the otolithic organ.
The aim of this chapter is to assess the vestibular function in patients affected by
relapsing vertigo of peripheral origin through vestibular evoked potentials, using
both techniques: VEMPs and EVG.
21.2 Materials and Methods
In this study, 52 patients were investigated (12 males, 40 females, mean age
43 ± 5.4 years). All patients presented with relapsing episodes of posterior semicir-
cular canal-type benign paroxysmal positional vertigo.
Relapsing paroxysmal positional vertigo (RPV) was defined as three or more
such episodes over a period of 12 months, with an interval symptom-free period of
at least 2 months. Although dizziness could persist in these patients, complete reso-
lution of the paroxysmal type of positional vertigo that followed a repositioning
maneuver was a condition of the study. All subjects were free of diseases of the
21 Vestibular Evoked Potentials in Relapsing Paroxysmal Positional Vertigo 225
external ear canal and middle ear. In order to exclude involvements of the canals or
the central vestibular pathways, they underwent to a complete neurootological
battery, as well as neuroimaging (MRI). In all considered subjects these tests
resulted as normal.
Out of the 52 patients suffering from RPV, 11 had no balance symptoms at the
time of examination and 41 continued to suffer from dizziness, despite successful
repositioning. The former were classified as asymptomatic (ASYM) and the latter as
symptomatic (SYMP). The symptoms in SYMP group were described as a momen-
tary instability, often associated with positioning or quick head movements. The
provocative maneuvers [14–16] did not evoke nystagmus or vertigo in all subjects.
For VEMP examination, patients were requested to be seated on a comfortable
chair keeping their head rotated to the opposite side of the stimulated ear to activate
the SCM. The active surface EMG electrode was placed on the SCM of the stimu-
lated side and referred to the ipsilateral clavicle, whereas a ground electrode was
fixed on the upper sternum. The vestibulocollic reflex was evoked by rarefaction
clicks (duration 100 ms, loudness 95 dB normal hearing level, rate 5 Hz) delivered
by a pair of headphones in two series for a total of 200 sweeps. Contralateral NB
masking 90 dB SPL was adopted. Four repetitions each side were performed. There
was no adjustment to individual hearing loss. A continuous noise of 70 dB was
presented to the contralateral ear. Recordings were performed using a standard clin-
ical evoked potentials averager (Nicolet CA2000) with time bases of 50 ms. The
responses to both series of sweeps were averaged twice to produce one grand aver-
age for each side and for each subject [17–19].
The parameters evaluated were:
• Presence/absence of the response
• Latency of the first positive (P1) and negative (N2) peaks
• Interpeak latencies (P1-N2)
• Amplitudes measured peak to peak (P1-N2)
Since the level of SCM contraction, which can vary remarkably between subjects,
influences the amplitude of the response, we concentrated on the latencies between
peaks. These latencies are more stable and better reflect the integrity of the vestibu-
lospinal pathway. Our normal latency ranges (25 subjects, 13 females and 12 males,
mean age 35.7 years) were 15.8 ± 1.5 ms for P1 and 25.4 ± 1.8 ms for N2 and inter-
peak latencies (P1-N2) 9.8 ± 0.8 ms (Fig. 21.1). Figure 21.1 shows a normal pattern
of VEMPs in A compared to an abnormal diagram in B characterized by increased
latency (P1 18.06 ms in B with respect to 15.57 in A) and decreased amplitude
(4 μV in B and 32 μV in A).
EVG was performed while the patient was sitting on a chair. For recording
evoked potentials, an extratympanic electrode was placed into the tympanic recess
of the ipsilateral ear, being fixed with a tape on the pinna as to prevent any move-
ment of the electrode during head tilts. The reference electrode was fixed on the
mastoid plane and the ground electrode on the forehead just below the hairline.
Tilting the head in roll and in pitch was employed to stimulate mainly the otolithic
organ. Tilting the head was swift (below 1 Hz) although not forceful. During tilting
raw data were collected and delivered to a data acquisition system with following
analysis (Inner Ear Analyzer, Enttex Pty. Ltd., Port Melbourne, Australia). EVG is
A B
–
10 µV n2
2 ms –85.42 µV, 22.36 ms
p1
52.96 µV,15.57 ms
n2
p1 –14.70 µV, 24.05 ms

18.21 µV, 18.06 ms
+
0.00 5.00 10.00 15.00 20.00 25.00 30.00 35.00 40.00 45.00
Latencies (ms)
Fig. 21.1 Left (A) and right (B) VEMPs. Normal morphology and latencies in the left evoked
VEM and reduced amplitude and increased latencies in the right evoked VEMP
based on an averaging procedure, and results are presented in boxplots, a visually

suitable format for physicians that permits to easily read the results. Boxplot
displays the interquartile range (seventy-fifth through twenty-fifth percentile).
For a detailed explanation of the technique, see Franz et al. 2003 and Franz et al.
2006 [11, 12].
Four recordings were performed: ipsilateral tilt to the electrode ear and contralat-
eral tilt away from the electrode ear (roll that could be mainly referred to the
response of the utricle) and forward tilt and backward tilt (pitch that could be mainly
referred to the response of the saccule). Each pair of tests (e.g., ipsi- and contralat-
eral tilts and forward and backward tilt) were compared in order to calculate a coef-
ficient, one mainly referred to sagittal responses (expressed as sacculus coefficient)
and the other mainly to lateral (expressed as utricle coefficient). In normal subjects
the interquartile range of ipsilateral head tilt is larger than the interquartile range of
contralateral head tilt, rendering a coefficient usually below 1 (range 0.5–1.1).
Similarly the interquartile range of forward head tilt is larger than the interquartile
range of backward head tilt, also rendering a coefficient usually below 1 (range
0.6–1.2) as calculated in a reference group of normals (12 males and 15 females,
mean age 32.5 years) (Fig. 21.2). Figure 21.2 shows a diagram of a normal EVG
which shows the responses of a subject without vestibulocochlear symptoms. Each
recording was preceded by a baseline assessment. This was an important measure-
ment and allowed comparison of base level of impedance. Provided similar
Date: 2007–04–19 Title: G.H. Swift head tilt left Patient name: G.H. Ear:Left
Utriculus coefficient: 0.79079 sacculus coefficient : 0.84309
1.5
1.0
º
º º
0.5
Box plot scaling
º
º
0.0
º
º
–0.5
º º
º
–1.0
–1.5
Baseline Ipsi Contra Forward Backward
Fig. 21.2 EVG boxplots. Averaging potentials recorded in different head positions are visually
compared to baseline value in order to provide an analog-scaled information regarding otolithic
function
impedance in ears, very small amplitude ranges or a significant interaural difference

of amplitude ranges (>30 %) is to be considered pathological.
Statistical analysis was performed with the standard student t-test (p < 0.05) and
the Pearson chi-square and Fisher’s exact tests.
21.3 Results
VEMPs were completely normal in nine ASYM patients. Four subjects revealed an
abnormal response in one ear, while only one patient revealed an abnormal response
in both ears (Table 21.1).
Although the two tests did not identify individual cases as normal or pathological
in the same way, the Pearson chi-square and Fisher’s exact tests showed comparable
results in cross correlations (Table 21.1).
The distribution of VEMPS and EVG abnormalities was comparable.
EVG was completely normal in all the ASYM patients. From the other group,
eight revealed an abnormal response in both ears, whereas one revealed an abnor-
mal response in one ear (Table 21.1).
The patients with abnormal EVG has been splitted according to the characteristic
of measured abnormalities. Table 21.2 evidences that vestibular endings involve-
ment is complex. In patients, a negative interaction between saccule and utricle thus
could be supposed.
In SYMP patients, VEMPs showed a bilateral delay in nine subjects, a left-right
asymmetry in 28. EVG results were more complex as pathological findings in
Table 21.1 VEMPs SYMP ASYMP Number of patients

and EVG distribution
VEMPs abnormal 37 2 39
in SYMP and ASYM
VEMPs normal 4 9 13
patients
EVG abnormal 39 0 39
EVG normal 2 11 13
Table 21.2 EVG abnormal findings

Number of patients
BAS (difference between baseline right and left values >30 %) 1
UTR (abnormal utricular coefficient) 11
SAC (abnormal saccular coefficient) 10
BAS + UTR (patients in which both abnormal utricular coefficient and 4
significative baseline value difference were revealed)
BAS + SAC (patients in which both abnormal saccular coefficient and 2
significative baseline value difference were revealed)
BAS + UTR + SAC (patients with abnormal utricular, saccular coefficients, 11
and significative baseline value difference)
UTR + SAC (patients with abnormal utricular and saccular coefficients) 13
Date: 2007–05–31 Title: G.L. Swift head tilt left Patient name: G.R . Ear: Left
Utriculus coefficient: 1.4 Sacculus coefficient: 1.28675
1.5
1.0 º º
º
0.5
Box plot scaling
0.0
º º
º º
–0.5
–1.0
º º º
–1.5
Fig. 21.3 In this case both macular coefficients are increased, specially the utricular one
SYMP patients could be subdivided into “utricular” (UTR), lateral tilt, and “saccu-
lar” (SAC), sagittal tilt, deficits (Table 21.2). In ten patients saccular responses were
abnormal. UTR responses were also abnormal in 11 patients, while a combined
UTR and SAC deficit was found in 13 patients (Fig. 21.3). This diagram shows an
abnormal UTR and SAC responses showing that both the coefficient were increased
but especially the “utricle” coefficient (1.4 compared to 1.28).
Date: 2007–05–10 Title: D.W. Swift head tilt right Patient name: D.W . Ear: Reft
Utriculus coefficient: 1.07895 Sacculus coefficient: 1.47368
1.5
1.0
0.5 º
º º º
º
Box plot scaling
0.0
–0.5 º º º º
º
–1.0
–1.5
Fig. 21.4 In this case very small amplitudes of the interquartile range are detected both in the
baseline assessment and in the SAC, sagittal, responses with increased coefficient (1.47). UTR,
lateral, coefficient is just within normal limits (1.07)
In one female patient, a significant baseline difference was found while the UTR
and SAC responses were normal. However, in two patients a significant baseline
difference was found while at the same time there was a deficit in the SAC, sagittal,
response, while in four patients it was the UTR, lateral, response. In 11 patients a
significant baseline difference was associated with a combined UTR and SAC defi-
cit. Figure 21.4 shows an EVG pattern characterized by very small amplitudes of the
interquartile range detected both in the baseline assessment and in the SAC, sagittal,
responses with increased coefficient (1.47). UTR, lateral, coefficient is just within
normal limits (1.07).
21.4 Discussion
In some whiplash cases, no evidence of residual involvement of every canal can be

revealed in those patients that present, during the course of their posttrauma life,
relapsing episodes of benign PPV, as the subjects investigated in our study. Current
neurootological tests in the diagnosis of vestibular diseases comprise electronystag-
mography, rotatory chair examination, caloric stimulations, and vestibular evoked
myogenic potentials (VEMPs). These tests have been refined over the years, but
among them VEMPs have become the most popular regarding vestibulospinal assess-
ment. Although it is a multineuron reflex test, suggesting little specificity, there is gen-
eral consensus that it gives accurate data regarding the saccule in the otolithic organ.
VEMPs when altered allow to explain residual and relapsing symptomatology

with a remaining macular deficit as the most obvious cause or as an inferior vestibu-
lar nerve or vestibular nuclei involvement. In some cases, as in the patients that we
were interested in, both neurootological and neuroimaging test are normal.
VEMPs may be considered a specific test of sacculo-spinal pathway even they
are not able to distinguish between peripheral (saccule, inferior vestibular nerve,
vestibulospinal tract) and central (vestibular nuclei) involvement [20–22].
In our patients VEMPs showed abnormalities in the largest part of SYMP patients
(90.24 %).
EVG results in this study revealed the same percentage abnormalities, but it
showed that about half of the SYMP patients had an abnormal UTR, lateral,
response. This raises the hypothesis that abnormal responses of the utricle must be
part of the overall response pattern in PPV, at least in the relapsing patients. It is
known that during head tilt, both canals and maculae are stimulated, but Franz [12]
assumed that responses collected through the extratympanic electrode were not con-
taminated by responses from the semicircular canals, as tilting the head is not per-
formed in the optimal plane to stimulate this part of the inner ear. In addition, tilting
the head is performed below a frequency of 1 Hz, which will avoid contamination
by responses from the semicircular canals [23].
Anyway, a cross-coupled interaction may be not excluded due to the plasticity
of the vestibular end organs, but this is out of the clinical interest regarding RPV
functional assessment. In fact the main aim of vestibular investigation in this field
of application is to document a disorder of the vestibular end organs as basis of
the relapsing vertigo and residual unsteadiness. These data suggest that RPV
could not be purely depending on sagittal tilt-sensitive receptors (mainly the sac-
cule), and we can speculate, at least for what our experience attains, that in some
patients there is also a disorder of the lateral tilt-sensitive receptors (mainly the
utricle).
With the introduction of EVG, a single neuron reflex test has become available
promising more information regarding vestibular end organs function.
As it is difficult for some whiplash patients to tilt the head, artifacts by muscle
activity could become a problem. These are also avoided by using a very slow tilt of
the head. Otherwise looking at the raw-recorded data these artifacts can be recog-
nized. Typically muscle activity is detected by excessive voltage changes far beyond
the regular appearing responses of the vestibular nerve. These excessive voltage
responses can be easily removed before the analysis.
Limitation of EVG application can be a discomfort while inserting the electrode
into the tympanic recess. If necessary, the discomfort can easily be overcome by
placing a small cotton ball soaked with cophenylcaine into the tympanic recess for
5 min. This will give enough anesthesias to go ahead with EVG testing, and it does
not interfere with the vestibular nerve response. Conductive hearing loss has no
influence on EVG recording and, even if it was not our cases, EVG may be per-
formed also with tympanic membrane perforation. Attention in the evaluation of
data has to be paid if granulomatosis or cholesteatoma is present into the eardrum
because impedance may be disturbed.
Conclusions
Vestibular potentials, in general, are specifically necessary to investigate residual
vestibular impairment in still symptomatic patients when presenting relapsing
benign PPV [24, 25]. VEMPs are well-established technique able to document
vestibular involvement in the largest part of patients. EVG, an innovative exami-
nation technique, promises specific information about the status of the utricle
and saccule, and possibly allowing detection of vestibular nerve degeneration.
Comparison between VEMPs and EVG provides specific differential diagnosis
between pure peripheral (EVG abnormal) and mixed involvement (VEMPs
abnormal and normal EVG). Furthermore, the combination of both vestibular
potentials may suggest useful information regarding vestibular end-organ func-
tion, at least in patients.
References
1. Caruso G, Nuti D (2005) Epidemiological data from 2270 PPV patients. Audiol Med 3(1):
7–11
2. von Brevern M, Radtke A, Lezius F, Feldmann M, Ziese T, Lempert T, Neuhauser H (2007)
Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol
Neurosurg Psychiatry 78:710–715
3. Bickford RG, Jacobson JL, Cody DTR (1964) Nature of averaged evoked potentials to sound
and other stimuli in man. Ann N Y Acad Sci 112:204–223
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cortical potentials to sound in man. Ann Otol Rhinol Laryngol 73:763–777
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Laryngoscope 79:400–416
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tion: its relation to the saccule. Ann Otol Rhinol Laryngol 80:121–131
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N Y Acad Sci 1039:54–67
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evoked potentials. Neurology 64:1682–1688
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542–544
10. Wang SJ, Jaw FS, Young YH (2013) Optimizing the bandpass filter for acoustic stimuli in
recording ocular vestibular-evoked myogenic potentials. Neurosci Lett 542:12–16
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Curr Opin Neurol 26(1):74–80
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vertigo. Int Tinnitus J 9:92–96
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Int Tinnitus J 2:31–39
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Whiplash Effects on Brain:
Voluntary Eye Movements 22
M. Spanio, S. Rigo, and D.C. Alpini
22.1 Introduction
Saccades and smooth pursuit eye movements play an important role in the balance
system. Essentially their aim is to free foveate animals from the slavery of oculomo-
tor reflexes, such as vestibulo-ocular reflex (VOR) and optokinetic nystagmus
(OKN). These voluntary eye movements enable the gaze to be rapidly redirected
(saccades) or to slowly follow (smooth pursuit movements) new targets even when
the head or surroundings are moving.
Saccades usually occur during VOR and OKN in order to automatically reset
slow eye drift caused by vestibular or optokinetic stimuli and bring the gaze to the
incoming scene, thus they have come to be known as nystagmus quick phases.
Moreover, saccades can help an oculomotor system which has been impaired by a
pathology and override its resulting limitations. For instance, an abnormal smooth
pursuit may present with saccades, seen on the eye record as a cogwheel shape,
which enhance global oculomotor response gain [1]. Even in labyrinth defective
patients, saccades represent a compensatory mechanism, taking on the role of the
defective VOR [2].
The smooth pursuit system is perhaps involved in evoked nystagmus visual
suppression, a function frequently investigated in clinical assessment of
visual-vestibular interaction.
M. Spanio (*)
“Salus” Private Hospital, via Bonaparte 4-6, 34123 Trieste, Italy
e-mail: cdc@salustrieste.it
S. Rigo
Otorhinolaryngology, Via del Coroneo, 32, 34133 Trieste, Italy
e-mail: rigostefano2@libero.it
D.C. Alpini

234 M. Spanio et al.
Therefore saccadic and smooth pursuit systems assist correct behaviour of the
balance system, and, when affected by neurological lesions, they might lead to bal-
ance impairment, causing blurred vision and dizziness.
Saccadic and smooth pursuit are very complex oculomotor systems whose
mechanisms have not yet been completely understood. As already stated the aim of
a saccade is to quickly move the gaze onto a new visual target, therefore the stimu-
lus consists in a gap between fovea and retinal target position, whereas the aim of a
smooth pursuit movement is to follow a moving object, and here the stimulus con-
sists in a velocity retinal slip between fovea and target.
The neural pathways of the two systems are completely different, but essentially
they extend from cerebral cortex to brainstem oculomotor nuclei, passing through
the cerebellum.
Therefore abnormalities of saccades or smooth pursuit movements are con-
sidered a precise and sensitive marker of a central nervous system (CNS)
pathology [3].
To record and analyse these ocular movements, we require special investigative
techniques and a well-equipped laboratory.
In a clinical environment, visual stimulation is usually provided by a LED array,
and horizontal binocular movements are collected by means of DC-EOG and
Ag-AgCl electrodes. As for the saccadic test, the subject is presented with predict-
able or unpredictable target jumps of several amplitudes (5–40°) in both directions
(rightwards and leftwards).
As for smooth pursuit the subject is studied by using continuous target movements
with triangular, sinusoidal or ramp patterns. Normally stimulus peak velocities of
20–40°/s are utilized.
Eye movements in saccadic tests are usually low-pass filtered at 50 Hz and
sampled at 250 Hz, whereas data from smooth pursuit tests are low-pass filtered at
10 Hz and sampled at 50 Hz. Butterworth 18 dB/oct low-pass filters and 12-bit AIO
conversion are used.
The most modern eye movement recording is video-oculography (VOG). A video
camera records directly the movements of the eyes and a computer analyses the data
obtained in this way. According to Pietkiewicz et al. [4]., with respect to the EOG,
VOG should be recommended in preference as the valuable method to assess ver-
tigo and to discriminate between the peripheral and the central vestibular lesions
but, for the purpose of WAD evaluation, informations about oculomotor system
involvement are comparable.
Analysis of saccadic movements is in two steps: first, a morphological evalua-
tion of the global eye movement response to each target jump (overshoots, postsac-
cadic drifts, etc.) and, second, an automatic/interactive identification of the start and
end points of each saccade, followed by an automatic evaluation of the saccadic
parameters (latency, amplitude, duration and peak velocity) for statistical analysis.
Saccadic abnormalities are evaluated taking into account the direction and the
amplitude of target displacement.
Analysis of the smooth pursuit responses is also in two steps: first, a morphologi-
cal evaluation of the global eye response (both the smooth and saccadic components
22 Whiplash Effects on Brain: Voluntary Eye Movements 235
are investigated) and, second, evaluation of the gain and the temporal shift of the
smooth component by cross-correlating the velocity of this component with that of
the stimulus.
Although there is still debate as to its significance, a widespread clinical applica-
tion of investigating the smooth pursuit system consists of a per-rotatory nystagmus
visual suppression test. The subject is rotated in darkness and asked to fix on a dim
light rotating with him. With a healthy CNS the visual system can suppress per-
rotatory nystagmus down to 30 % of the initial value or even lower.
22.2 Whiplash-Associated Saccades and Pursuit Disturbances
In whiplash injuries, it has been calculated that the sudden jerk of the neck can
cause an elongation of the cervical columna up to 5 cm and thus an elongation of the
brainstem [5]. This event can lead to, besides a wide range of lesions in the columna,
nerve roots and medulla, even lesions in the brain stem, cerebellum and oculomotor
system. Several authors have investigated the saccadic and smooth pursuit systems
in whiplash patients.
Oosterveld et al. [6] submitted 262 patients, chronically suffering from the after-
effects of whiplash to an extensive vestibular and oculomotor examination. Some
85 % of the patients complained of light-headedness, spinning or floating sensa-
tions. Disturbances in visual pursuit movements were found in 113 patients (43 %)
and in visual suppression tests in 97 patients (37 %), proving the presence of both
cerebellar and brainstem pathology. However, a large number of patients (63 %)
also had a spontaneous nystagmus of more than 5° Is, interpreted by the authors as
a sign of central origin, which might interfere with smooth pursuit performance.
In 41 patients oculomotor tests repeated l year later showed no significant
improvements.
A high correlation between symptoms and oculomotor abnormalities has been
found by Hildingsson et al. [7]. They examined the oculomotor function in 39 con-
secutive whiplash patients 6 months or more after the trauma. Twenty patients com-
plained of chronic and disabling symptoms, such as neck ache, neck stiffness,
headache, shoulder and arm pain. Two patients had vertigo or dizziness. Visual
symptoms, often blurring of vision, as well as auditory symptoms were present in
15 patients. No difference in visual tracking was noted between 19 asymptomatic
patients and control group subjects, whereas an oculomotor dysfunction was noted
in 18 of 20 patients with persisting symptoms of a soft-tissue injury of the cervical
spine. Four patients had pronounced abnormalities, and 14 had moderate oculomo-
tor dysfunction.
In particular, smooth pursuit was abnormal with reduced velocity gain in 14
patients (in 12 asymmetrically) and with an increase in superimposed saccades in
16 patients (in 13 unilaterally). The saccades were hypometric in nine patients. Six
patients had poorer accuracy and maximal velocity of the saccades, and five of these
patients also showed latency prolongation. In general, patients with chronic symp-
toms had prolonged saccadic latency (p < 0.001).
Patients with more pronounced smooth pursuit abnormalities presented with sac-
cadic dysfunction. None of the patients with saccadic dysfunction had normal pursuit.
The authors suggest that the proprioceptive system in the cervicocranial area is affected
in 14 patients with moderate oculomotor impairment and that in four patients with
pronounced oculomotor abnormalities, the brainstem and cerebellum are affected.
Observations of Hildingsson et al. [7] demonstrate that sometimes oculomotor
system disorders can occur at a later date. The authors investigated 40 consecutive
whiplash patients. The most frequent acute symptoms after injury were aching
and stiffness in the neck and headaches, followed by dizziness and shoulder pain.
The initial oculomotor tests, performed within 3 months of the accident, were
pathologic in eight patients. The follow-up test, on average 15 months after the
accident, remained pathologic in the eight patients and a further five patients had
changed from normal to pathologic test results. All the 13 patients with oculomo-
tor dysfunction had disabling symptoms. In six patients smooth pursuit eye move-
ments were abnormal with reduced velocity gain and with increased superimposed
saccades.
In all 13 patients the saccades showed low peak: velocity and prolonged laten-
cies. Three patients suffered pronounced abnormalities affecting both smooth pur-
suit and saccades.
Wenngren et al. [8] investigated the prevalence of brain/brainstem dysfunction
after acute whiplash trauma (grades II and III according to the Quebec Task Force
Classification on whiplash-associated disorders) and the possible correlation
between the development of chronic symptoms and objective findings from eye
motility tests. They used oculomotor tests in a sample of prospective whiplash
trauma patients who were followed up for 2 years after the trauma. The initial test
results did not reveal any prognostic clinical signs for the tested group as a whole,
but they could discriminate some patients with clinical symptoms and signs paired
with pathologic test results. Over time, some patients normalized clinically and
their test results improved, while others deteriorated clinically and their test results
were worse at the 2-year investigation.
Further support to the involvement of oculomotor systems in whiplash comes
from the Kogler et al. study [9]. The authors investigated 25 acute whiplash patients
using, among other tests, smooth pursuit tests, saccadic tests and per-rotatory nys-
tagmus visual suppression tests. The patients were consecutive which meant that
even lighter trauma could be included in the study.
They were checked after 3, 6 and 9 months. At the first consultation about half of
the patients had disturbances. The results are interpreted as indicating that patho-
logical visual suppression and especially defective smooth pursuit ability may point
to a chronic lesion of the brain stem. The patients concerned also had vertigo and
unsteadiness. However there was no correlation between symptoms and pathologi-
cal saccade tests.
In patients referred to our hospital for whiplash symptoms, we began a study of
the VOR, and of a possible cervico-ocular component, by means of active and pas-
sive head movements. Out of these patients 14 were also submitted to saccade and
smooth pursuit tests. The age of the patients ranged from 51 to 24 years (mean age
Table 22.1 Whiplash patients: oculomotor results

Smooth pursuit VOR/Hz
Saccades (gain) (gain/phase)
Main
sequence Latency Metricity Shape 20 % 40 % Horiz. Vert.
1 N Increased N N 0.88 0.83 0.82/−5 1.05/−3
2 N N N N 0.97 0.85 0.75/3 0.95/−5
3 N N N N 0.98 0.80 0.73/−9 0.98/−6
4 PV ⇑ d ⇓ N N N 0.90 0.75 0.96/−6 0.91/−15
5 N N N N 0.89 0.82 0.75/−6 1.10/−11
6 N N N Overshoots 0.97 0.87 0.75/−6 1.15/−13
7 N N N N 0.90 0.82 0.80/2 1.15/−40
8 N N N N 0.98 0.86 0.67/−5 0.65/−8
9 PV ⇑ d ⇓ Increased N N 0.99 0.68 1.07/−6 1.10/−10
10 N N Hypometria N 0.94 0.62 0.93/−8 0.95/−13
11 PV ⇓ Increased Hypometria N 0.90 0.59 0.90/−2 0.89/−9
12 PV ⇓ N N N 0.78 0.65 0.65/−9 1.05/−10
13 N N N N 0.85 0.78 0.69/−5 0.52/−10
14 PV ⇑ d ⇓ Increased N N 0.70 0.55 0.50/3 0.89/−4
PV peach velocity, d duration, N normal parameters
32.8 years); older patients were excluded in order to avoid impairment of saccadic
and smooth pursuit performances due to aging or pathologies. Seven patients com-
plained only of cervicobrachialgia or headache; seven complained also of dizziness
and unsteadiness. All the patients were examined within a week of the accident.
Even light trauma was included. The test results are reported in Table 22.1.
Saccade abnormalities appeared mostly in the symptomatic group, but even in
some asymptomatic patients. A lower smooth pursuit gain was present only in
symptomatic patients. The symptomatic group often presented a lower VOR gain.
Only one asymptomatic patient presented a large phase lag of vertical VOR.
The number of patients examined is too small to draw a definite conclusion;
nevertheless a relevant difference between our groups is the presence, in symptom-
atic patients, of an abnormality in at least one out of the three systems investigated.
This might justify the balance disturbances the patients complained of. Nevertheless,
the absence of a precise correlation between saccade abnormalities and symptoms,
as found also by Kogler et al. [9], reduces the weight of saccade abnormalities on
the balance. Even an isolated, but marked, saccade slowness cannot completely
account for patients’ complaints. Actually a low gain in the VOR or smooth pursuit
has, on balance, greater effect than saccade slowness. A summary of the above-
mentioned studies on whiplash injuries shows that saccade and smooth pursuit
abnormalities are often present in symptomatic patients.
If the impairments of saccades and smooth pursuit movements are considered a
marker of a CNS pathology, how can their presence be explained in subjects affected
by a soft-tissue injury of the cervical spine without assuming a contemporary head
injury? Patients who received head trauma must have been excluded from data anal-
ysis. Therefore oculomotor abnormalities reveal damage of the CNS probably due
to pull, stretch and pressure of the medulla oblongata, brainstem and cerebellum
during the sudden jerk of the head [10–12].
A different hypothesis has been proposed by Hinoki [13]. In patients with
whiplash injury, there might be an overexcitation of the cervical and/or lumbar
proprioceptors on the one hand and a dysfunction of the CNS, such as the hypo-
thalamus, the brainstem and the cerebellum, on the other hand.
These two factors cause imbalance by means of a trigger-and-target relationship
in which the above proprioceptors act as a trigger and the CNS acts as a target. This
hypothesis of a proprioceptive trigger, according to Hildingsson et al. [7], could
explain even saccade and smooth pursuit abnormalities.
Nevertheless, a further element should be taken into account with regard to this
type of oculomotor test. Saccades and smooth pursuit performances depend on
cognitive functions to a large extent. Radanov et al. [14] evaluated the cognitive
functions in whiplash patients and found they were impaired in terms of attention
and speed of information processing. [15, 16].
These observations could justify some abnormalities: for instance latency
increase in the saccades and gain decrease in smooth pursuit movements.
In conclusion, the high incidence of saccades and smooth pursuit abnormalities
in whiplash patients highlights the importance in investigation of whiplash injuries
of oculomotor voluntary tests in order to prove the seriousness of the trauma.
Nevertheless, these tests must be integrated into a larger clinical protocol aimed at
the assessment of vestibular and optokinetic systems and postural control.
Abnormalities in both saccadic and smooth pursuit systems may account for
patients’ complaints about balance only when the other tests provide normal results.
The outcome of patient follow-up using these tests can be very useful both for
patient control and medical legal purposes.
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Whiplash Effects on Brain: Optokinetic
Nystagmus and Visuo-Vestibular 23
Interaction
A. Salami, M.C. Medicina, and M. Dellepiane
23.1 Introduction
Different papers [1–5] suggest the existence of complex peripheral and, overall,
central alterations in the vestibular system as a consequence of a trauma in the cer-
vical portion. Thus we studied optokinetic and visual vestibular system behavior in
subjects who previously underwent a cervical whiplash injury. The results of our
research could be both interesting from a clinical point of view and useful for medi-
colegal goals. Our methods could be suitable for pointing out alterations in central
sites as it is known that the nystagmus resulting from the contemporary optokinetic
and roto-acceleration stimulation with counterdirectional nystagmus is significantly
weakened in brain stem and cerebellar lesions and more widely in the presence of
lesions in the posterior cranial fossa [6–9]. The visuo-vestibular interaction has not
yet been adopted in the study of cervical whiplash injury.
23.2 Methods
The investigation was carried out on 32 subjects of age between 21 and 48 (18 men
and 14 women) who had undergone a cervical trauma for a traffic accident with
whiplash injury (Table 23.1). Thirteen subjects were examined within the third
month following the accident (1st group), six subjects between the third and the
sixth month (2nd group), and 13 subjects later than 6 months up to 24 months (3rd
group). It is important to note that we observed a spontaneous horizontal nystagmus
in three subjects (one for each group) with an incidence of 9.3 % out of the total.
The recording of ocular movements was done by the usual method using an
eight-channel Tonnies electronystagmograph. The subjects were sitting with their
heads still, on a Tonnies rotatory chair Pro model, which was placed in the middle
A. Salami (*) • M.C. Medicina • M. Dellepiane

Otorhinolaryngology, “San Martino” Hospital, Largo Rosanna Benzi 10, 16132 Genoa, Italy
e-mail: http://www.otorinoangelosalami.com/contatti

242 A. Salami et al.
Table 23.1 Complaints after Number %

cervical whiplash injuries
Headache 21 65.6
in 32 patients
Subjective vertigo 13 40.6
Objective vertigo 4 12.5
Floating sensation 15 46.8
Tinnitus 14 43.7
Tinnitus and hearing impairment 5 15.6
Neck pain 13 40.6
Fig. 23.1 Rotatory

cylindrical chamber. The
Tonnies rotatory chair system
Pro in the middle
of a rotatory cylindrical chamber with a diameter of 2 and 1.9 m high. Its white
internal area was covered with 32 black vertical contrasts (Fig. 23.1), each one
9.32 cm wide and with an angle of 5.61°.
The rotatory cylinder was lighted from above by a 100 W lamp and was driven
by a direct current engine able to reach the desired turning speed (clockwise and
counterclockwise of up to 2,000/s maximum speed, with preset acceleration ranging
from 1° to 20°/s2).
23 Whiplash Effects on Brain: Optokinetic Nystagmus and Visuo-Vestibular Interaction 243
Each patient was exposed to:

1. Postrotatory vestibular stimulation (VOR, vestibular ocular reflex): with stop
test, eyes open in the dark at an angular velocity of 900/s which was subliminally
reached clockwise and counterclockwise.
2. Optokinetic stimulation (OKN, optokinetic nystagmus) “stare type” with a cyl-
inder rotation velocity of 300/s for 60 s with clockwise and counterclockwise
rotation.
The length of 60 s was chosen because we thought that VOR could sometimes
prevail over OKN. In this respect, our previous research on visuo-vestibular
interaction [10] had shown that in cases of lack of VOR substitution by OKN,
sometimes it took more than 20 s for the appearance of OKN.
3. Contemporary postrotatory vestibular and optokinetic stimulation (VVOR,
visuo-vestibular ocular reflex) at the postrotatory stop: the light was turned on
and we effected optokinetic stimulation with a cylinder (and optical contrasts)
rotation capable of inducing an OKN which was beating on the opposite side of
the postrotatory vestibular nystagmus.
We took into account the fundamental parameter nystagmus “gain” as the ratio
between the angular velocity of nystagmus slow phase and the stimulation velocity.
VOR mean gain was calculated on the first three beats; OKN mean gain was calcu-
lated on the beats in the first 20 s; VVOR mean gain was calculated:
1. On the first three beats during the first 20 s of optokinetic stimulation, when the
resulting nystagmus was beating in the OKN direction.
2. Only on the first three beats, when the resulting nystagmus was beating in the
VOR direction.
The results were compared with the ones we obtained in a group of seven normal
subjects, ages 28–36, and statistically evaluated (mean difference) by t-test.
23.3 Results
The results (Tables 23.2 and 23.3 and Figs. 23.2, 23.3, 23.4, and 23.5) can be
summed up as follows:
• VOR: none of the normal or pathological subjects showed any significant differ-
ences between the sides (p > 0.05). In pathological subjects mean gain decreased
Table 23.2 Mean with standard deviation of the mean gain

VVOR VVOR
VOR OKN OKN DIRa VOR DIRb
(3 beats) (20 s) (3 beats) (20 s) (3 beats)
Normal subjects 0.47 ± 0.08 0.46 ± 0.07 0.25 ± 0.09 0.32 ± 0.02 (−)
1st group (0–3 month) 0.34 ± 0.11 0.64 ± 0.18 0.15 ± 0.05 0.25 ± 0.08 0.12 ± 0.08
2nd group (3–6 month) 0.45 ± 0.12 0.73 ± 0.09 0.22 ± 0.14 0.29 ± 0.19 0.18 ± 0.13
3rd group (over 6 month) 0.38 ± 0.11 0.71 ± 0.11 0.28 ± 0.11 0.3 ± 0.10 0.18 ± 0.14
a
OKN DIR, nystagmus beating in the OKN direction
b
VOR DIR, nystagmus beating in the VOR direction
Table 23.3 Significance test (t-test) between normal subjects and whiplash patients
VOR ON VVOR OKN Direction
(3 beats) (20 s) (3 beats) (20 s)
Normal vs. 1st group p < 0.05 p < 0.05 p < 0.01 p > 0.05
Normal vs. 2nd group p > 0.05 p < 0.01 p > 0.05 p > 0.05
Normal vs. 3rd group p > 0.05 p < 0.01 p > 0.05 p > 0.05
VOR VOR
OKN Stare OKN Stare
VOR VOR
Fig. 23.2 Normal subject. From top to bottom: the postrotatory nystagmus (VOR) in the dark at
the constant angular velocity of 90°/s with clockwise and counterclockwise chair rotation; optoki-
netic nystagmus “stare type” (OKN) with the cylinder rotatory constant velocity of 30°/s for 60 s;
and visuo-vestibular ocular reflex (VVOR) with a cylinder rotation which caused an OKN beating
on the opposite side of the postrotatory vestibular nystagmus. VVOR with counterdirectional VOR
and OKN always evokes a nystagmus beating in the OKN direction
in all three groups compared with normal ones (Table 23.2), but it was statisti-
cally significant (p < 0.05) only in the subjects of the first group (Table 23.3), that
is, in those subjects who underwent the trauma more recently.
• OKN: none of the normal or pathological subjects showed any significant differ-
ences between the sides (p > 0.05). In pathological subjects mean gain increased—
with respect to normal ones—in all three groups (Table 23.2), with a significant
increase (p < 0.05) in the first group and highly significant increase (p < 0.01) in
the second and third groups (Table 23.3).
• VVOR: in normal subjects VVOR always beats OKN direction, with a mean
gain on the first three beats slightly inferior to the one calculated during the first
20 s (Table 23.2).
In 16 cases the pathological subjects’ VVOR beats in the same direction of nor-
mal subjects (six in the first, four in the second, six in the third group), with a mean
gain on the first three beats which only in the first group showed a statistically sig-
nificant variation (decrease) (p < 0.01) compared with normal subjects (Table 23.3).
In the three groups of pathological subjects, the mean gain, during the first 20 s,
showed a decrease compared to normal, but it was not statistically significant
(Table 23.3).
In the remaining 16 cases (seven in the first, two in the second, seven in the third
group), VVOR beats in the same direction as VOR for a variable length of 3–15 s
(Figs. 23.3 and 23.4) with a mean gain on the first three beats always highly inferior
to VOR ones; VVOR beating in the VOR direction was followed by a variable
10º
VOR
2s
VOR
OKN
OKN
vVOR
vVOR
Fig. 23.3 Patient of the first group. From top to bottom: postrotatory nystagmus (VOR) and opto-
kinetic nystagmus “stare type” (OKN and visuo-vestibular ocular reflex). Note increase of OKN;
VVOR is characterized by a nystagmus beating in the VOR direction for about 10 s. After a vary-
ing period of ocular immobility, a nystagmus beating in the OKN direction appeared. The vertical
arrows point out the chair stop. For further information, see Fig. 23.2
VOR 10º
2s
VOR
OKN
OKN
VOR
VOR
Fig. 23.4 Patient of the second group
period (a few seconds) of ocular immobility and then by a nystagmus beating in the
OKN direction (Fig. 23.5).
23.4 Discussion
The results of our research pointed to a statistically significant decrease of VOR and
VVOR mean gains (beating in the OKN direction calculated on the first three beats)
compared with normal subjects in the patients of the first group and a significant
10º
VOR
2s
VOR
OKN
OKN
VOR
VOR
Fig. 23.5 Patients of the third group
increase of OKN mean gain in the patients of all the three groups. Furthermore, at
VVOR, immediately after the stop, we observed a nystagmus beating in the VOR
direction which lasted from 3 to 15 s in 16 patients out of 32 (seven in the first, two
in the second, seven in the third group).
In 1968 and in 1970, Miura et al. [11, 12] observed that cervical trauma of a
certain extent (about 7 G) which was experimentally induced in rabbits determined
either microcirculatory alterations of brain stem and the superior portion of the
spine or circulatory disturbances of the peripheral labyrinth. By analogy we can
assume that the significant decrease of VOR mean gain that we observed in patients
with cervical whiplash injury belonging to the first group could be due to labyrinthic
alterations subsequent to circulatory labyrinthic alterations.
The possibility of damage, also minor, to peripheral vestibular structures as a
direct consequence of cervical whiplash injury is also suggested by Chester [13]
and by Brandt [1], as well as on the basis of the experimental data of Schuknecht
and colleagues [14], who found a degeneration of Corti’s organ and secondary of
the pertaining acoustic fibers; these data could be taken into account in trying to
explain, partially at least, the vestibular and audiological complaints (particularly
hearing loss and tinnitus) referred to by some of our patients (Table 23.1).
As to the significant increase of OKN mean gain that we observed in all three
groups, our results agree with those obtained by other authors [15]. Therefore, tak-
ing into account the importance either of vestibular nuclei in the production of OKN
[45, 35] or of the pathway (even if it is not completely known) which is crossed by
optokinetic impulses at the subcortical site (tectum region and pontinus tegmen)
[16, 17] and if we also consider that the cerebellar nodulus and flocculus receive
visual and proprioceptive vestibular inputs [18–20], we may conclude that OKN
increase in cervical whiplash injury is determined by (a) pathological reactivity of
vestibular nuclei caused by cervical proprioceptors “overexcitation” [21]. The con-
nections of cervical proprioceptors with brainstem and particularly with vestibular
nuclei and reticular structure are already known [22], and (b) an altered microcircu-
lation of brain stem [23] and/or by a neurological-vascular friction which may cause
functional disorders of CNS and in particular of brain stem structures in cervical
whiplash injury [24].
As to VVOR, it is known that the optokinetic-vestibular interaction with coun-
terdirectional VOR and OKN evokes, in normal subjects, a nystagmus which is
always beating in the OKN direction, with a mean gain decrease in relation to OKN.
Our present results confirm these data as a further demonstration that a periph-
eral labyrinthic excitation, evoked by any technique and even if it is intense, induces,
in normal subjects, a nystagmus which is always overcome by a contrasting OKN.
Nevertheless in six cases out of 13 patients belonging to the first group, VVOR
appeared with a nystagmus beating in the OKN direction, but with a mean gain—on
the first three beats—which was significantly decreased compared with normal sub-
jects. Finally in 16 out of 32 cases of the three groups (seven in the first, two in the
second, and seven in the third group), VVOR was characterized by a nystagmus
beating in the VOR direction.
Numerous studies of animal anatomy and physiology showed the importance of
the cerebellar flocculus in the working out of visual vestibular interaction [25] and
its influence on central velocity storage mechanism [26–28]. Therefore this struc-
ture is likely to be involved as a consequence of cervical whiplash injury, and an
alteration may occur in the transmission of inputs coming from the caudal portion
of inferior olive nucleus. We may also face an alteration of the flocculus control
function on vestibular inputs, as Miles and Fuller [29] have already showed.
From a clinical point of view, these data confirm the importance of ENG exami-
nation in cervical whiplash injury. The alterations of OKN (statistically significant
increase of mean gain in all three groups of patients) and of VVOR (nystagmus
beating VOR direction) show—without reference to its pathogenetical origin—the
presence of lesions, especially of central type and more specifically regarding brain
stem and cerebellum. It is evident that these results are interesting from a medicole-
gal point of view. Therefore we can repeat Oosterveld and colleagues’ words: “In
cases where legal medicine is involved, the outcome of an extensive nystagmo-
graphic examination can be of utmost importance both for the doctor and for the
patients.”
References
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dromes. Springer, London, p 281
2. Compere WE (1966) Electronystagmographic findings in patients with “whiplash injuries”.
Laryngoscope 78:1226
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spine injury. Acta Orthop Scand 60:513
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and visual-vestibular interaction in subjects with “whiplash injuries”. Acta Otorhinolaryngol
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Abducting Interocular
Ophthalmoplegia After Whiplash 24
Injuries
D.C. Alpini, A. Cesarani, and E. Merlo
24.1 Introduction
Internuclear ophthalmoplegia (INO) is a well recognisable disorder of horizontal

eye movements, and it is a common finding in neurological disorders [1]. INO is
due to a functional impairment of the medial longitudinal fascicle (MLF) ipsilateral
to the medial rectus paresis. Generally INO is characterised by the impairment of
adduction of the eye on the side of the impaired MLF and abduction overshoot. The
electro-oculographic saccadic and gaze nystagmus patterns are typical.
In whiplash injuries, ocular motor disturbances are frequent also in those
patients in whom a head trauma did not occur [2–4]. In rare cases [5] eye movement
disorders are characterised by ocular conjugate movement impairment sometimes
as typical INO, sometimes as isolated abducens palsy.
With a certain frequency, we observed “atypical” abducting ophthalmoplegia pat-
tern, characterised by bilateral impairment of the velocity of the abducting eye [6–8].
This finding was described by Lutz [9], who proposed the existence of an abduc-
tion paresis of prenuclear origin (posterior internuclear ophthalmoplegia, pINO).
D.C. Alpini (*)

A. Cesarani
Milan, Italy
E. Merlo
ENT Department, Azienda Ospedaliera Ospedale di Circolo di Busto Arsizio,
Saronno e Tradate, Milan, Italy
Department of Otolaryngology, Tradate Hospital,
Piazza 24 Maggio, 1, 21049 Tradate Varese, Italy

As his basic neuroanatomical assumptions were erroneous, the existence of this

kind of INO remained controversial, and papers in the literature are quite rare.
Abduction INO differs from abducens nerve palsy in several aspects, such as
absence of strabismus and diplopia in the primary position and adduction nystag-
mus of the contralateral eye [10–14].
The aim of this chapter is to report the frequency of abducting INO that occurred
in a group of patients after whiplash injuries without head trauma and to discuss
possible etiopathogenic mechanisms.
24.2 Material and Methods
Twenty-three consecutive subjects were investigated: 16 women and seven men

with mean ages of, respectively, 31.35 and 34.7 years (from 16 to 70 years).
Eye movements were recorded in DC by a computerised Nicolet Biomedical
Nystar electro-oculograph, using monocular electrodes. Eye movements were elic-
ited by means of a semicircular LED bar, and the following tests were performed:
• Horizontal and vertical random saccades from 6° to 32°
• Sinusoidal 0.2 and 0.4 Hz horizontal smooth pursuit and 0.2 vertical smooth
pursuit
• 400/s bidirectional horizontal OKN and 200/s vertical OKN
The following parameters were calculated:
• Saccades: delay, accuracy, number, performance index, and mean velocity at
each amplitude
• Smooth pursuit: gain, DC offset, total harmonic distortion, and maximum
velocity
• OKN: number of beats, frequency, maximum velocity, and gain
• Sinusoidal provoked nystagmus (0.5 Hz at 11.5 and 5.75°/s2) in the dark (VOR)
and in the light (VVOR): nystagmus frequency and mean slow phase velocity
(SPV) and VVOR gain (VVOR-SPVNOR-SPV)
24.3 Results
The presence of bilateral abducting eye slowing was evaluated comparing accuracy,
performance index and saccadic eye velocity with the normal values previously
calculated in a group of 25 normal adults. No patients showed slowing of the adduct-
ing eye or another pattern like typical INO.
Horizontal saccades revealed slowing of the abducting eye in eight patients
(ABD) (34.7 %): two men and six women with mean ages of 35.87 years (from 16
to 58 years).
The mean age of the group of patients without abducting slowing was 33.67 years
(from 19 to 70 years).
In Table 24.1 the distribution of altered neurological tests is shown. The percent-
ages of altered tests regarding patients with abducting eye slowing are referred to
alterations of parameters other than eye velocities, such as latency, accuracy, offset,
and directional preponderance.
24 Abducting Interocular Ophthalmoplegia After Whiplash Injuries 253
Table 24.1 Percentages ABD (%) No-ABD (%)

of pathological tests in
Horizontal saccades 62.5 20
patients with (ABD) and
Vertical saccades 25 26.6
without (no-ABD) abducting
interocular ophthalmoplegia Horizontal smooth pursuit 37.5 40
Vertical smooth pursuit 25 33.3
Horizontal OKN 25 20
Vertical OKN 0 6.6
VOR 37.5 40
VVOR gain 25 66.6
Horizontal saccades are altered in 62.5 % of ABD patients versus 20 % of the

other group. All the other ocular motor tests are altered in the same manner in the
two groups of patients (with exception of VVOR).
24.4 Discussion
Internuclear ophthalmoplegia can be attributed to a lesion of the MLF between the

levels of the third and sixth nucleus [15]. It has been assumed that the lesion affects
axons arising from cells in the paramedian pontine reticular formation (PPRF), but
this is not an accepted explanation for every case. In fact the impairment of move-
ment is variable, the most severe lesions causing complete loss of adduction beyond
the midline during contralateral gaze; in some cases the impairment also affects the
convergence mechanism, while in others convergence is normal.
Cogan [14] divided INO into anterior and posterior types according to whether
the convergence was normal or not, while Lutz [9] divided INO into anterior and
posterior according to whether the medial or the lateral rectus muscle was para-
lysed. If convergence is still possible, it seems to be difficult to distinguish mono-
lateral INO of abduction from abducens paralysis, while bilateral abducting INO
may refer only to a lesion of the internuclear fibres.
There has been little agreement on the location of the responsible lesion and the
pathophysiological explanation of abducting INO. Some authors [16], rejecting the
existence of a prenuclear abduction paresis, attributed such cases to the pontine
involving the abducens nerve along its infranuclear intrapontine course. Others [17]
postulated decreased excitation of the lateral rectus motor neurons due to a lesion of
prenuclear structures, that is, aberrant “pyramidal tract” fibres to the abducens
nucleus or the connection between the PPRF and the ipsilateral abducens nucleus.
An impaired inhibition of the antagonistic medial rectus muscle was discussed by
Collard et al. [18] suggesting an MLF lesion contralateral to the paretic eye.
Thomke et al. [13] demonstrated that the lesion is ipsilateral to the abduction
paresis at the upper pons or midbrain level. They also showed the existence of a
fasciculus near the MLF specific for inhibition of medial rectus. They stated that
ABD ophthalmoplegia is due to impaired inhibition of medial rectus tonic resting
activity following interruption of this para-MLF fasciculus.
In our opinion, despite the controversy about the physiopathology of abducting
ophthalmoplegia, the term of “abducting interocular ophthalmoplegia” is preferable
rather than the classical “internuclear”. In our experience this pattern is not rare, and
Fig. 24.1 A case of abducting interocular ophthalmoplegia following whiplash
if monocular ENG recording is routinely performed, it describes a third of the

patients suffering vertigo and/or dizziness after whiplash injuries, even without
minor or major head trauma.
In Fig. 24.1 a case of abducting interocular ophthalmoplegia following whiplash
is showed. The involved parameters are peak velocities/movement amplitude ratio
(the butterfly diagram) and the percentages of accuracy, comparing abducting and
adducting movements.
24 Abducting Interocular Ophthalmoplegia After Whiplash Injuries 255
The PI (performance index) refers to patient peak velocities compared to normal

values previously stored in the programme.
It is interesting to reveal that neuro-otological differences in the two groups of
patients concern, in an opposite way, horizontal saccades and VVOR. In fact in the
ABD group, horizontal latencies or adducting accuracies (parameters different from
those correlated to abducting eye slowing) were altered in 62.5 % versus 20 % of
the other subjects, while VVOR was normal in 75 % and altered in 66.6 % of no-
ABD patients.
In no case was adducting slowing recorded, and we know only one paper in the
literature describing INO after whiplash without head trauma [6].
If we hypothesise a brainstem lesion with para-MLF involvement due to neck
hyperextension, there will be no need to exclude the possibility of the neurologi-
cally most frequently occurring adducting ophthalmoplegia. Our cases are not mis-
diagnosed bilateral abducens palsy as described either on the basis of the clinical
considerations reported in the introduction or on the basis of ophthalmological
examination excluding abducens palsy.
In our opinion abducting interocular ophthalmoplegia has to be considered a
disorder of ocular coordination correlated to head-eye, according to Treleaven et al.
and Montfoort et al. [19, 20], and/or head-neck coordination disorders, according to
Kongsted at al. and Treleaven et. al. [21, 22], caused by whiplash. It must not neces-
sarily be correlated to a brainstem lesion.
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persistent whiplash associated disorders. Man Ther 16(3):252–257
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687–693
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Part IV
Treatment
Pharmacological Treatment
of Whiplash-Associated Disorders 25
(WAD)
E.A. Pallestrini, E. Castello, G. Garaventa, F. Ioppolo,

and F. Di Berardino
25.1 Introduction
The term ‘whiplash’ has been used to describe a mechanism of injury and the
various clinical manifestations as a consequence of the injury. Moreover, signs and
symptoms have been designated the ‘whiplash syndrome’. In 1995, the Quebec
Task Force (QTF) on Whiplash-Associated Disorders (WAD) adopted the following
definition of whiplash: ‘whiplash is an acceleration-deceleration mechanism of
energy transfer to the neck. It may result from rear-end or side-impact motor vehicle
collisions, but can also occur during diving or other mishaps. The impact may result
in bony or soft-tissue injuries (whiplash-injury), which in turn may lead to a variety
of clinical manifestations called Whiplash Associated Disorders’[1].
Whiplash patients can be classified according to severity of signs and symptoms.
The QTF-WAD classification system consists of five levels: WAD 0 indicates no
complaints or physical signs; WAD I indicates neck complaints but no physical
signs; WAD II indicates neck complaints and musculoskeletal signs (such as a
decreased range of motion or muscle tenderness); WAD III and IV indicate neck
complaints and neurological signs (WAD III) or fracture/dislocation (WAD IV),
respectively. The most common presenting symptoms following an acute motor
E.A. Pallestrini • E. Castello • G. Garaventa

I Division of Otolaryngology, Head and Neck Surgery,
“San Martino” Hospital, Genoa, Italy
F. Ioppolo (*)
00185 Rome, Italy
F. Di Berardino
Milan, Italy

260 E.A. Pallestrini et al.
vehicle collision were neck pain (88–100 %) and headache (54–66 %). Other symp-
toms were neck stiffness, shoulder pain, arm pain/numbness, paraesthesia, weak-
ness, dysphagia, visual and auditory symptoms and dizziness. In most cases, WAD
resolves quickly; 47 % of injured people return to normal activities within 4 weeks,
and only 2 % continue to be absent from pre-accident activities 1 year after injury.
Pharmacological treatment of acute WAD regards especially vertigo, dizziness,
neck pain, headache, nausea and unsteadiness. Vertigo, nausea and cervical pain are
very frequent in the acute and subacute [2] WADs; unsteadiness and diffuse (not
only cervical) spine pain are very usual in the chronic WADs [3, 4].
25.2 Whiplash-Associated Headache and Neck Pain
The main goal of treatment must be to kill the pain in order to avoid processes of
spinal and central sensitisations that may lead to chronic pain [5].
Paracetamol at the dosage of 1 g three times a day for 7/10 days is the first drug
of choice for pain relief. Paracetamol has to be preferred over other nonsteroidal
anti-inflammatory (NSAI) drugs, even if it has to be administered at high dosages.
Paracetamol and, in general, NSAI have to be combined with muscle relaxant sub-
stances. They can be divided into: (1) drugs active on CNS (mephenesin, carisopro-
dol), (2) drugs with spinal actions (baclofen), (3) drugs active on the muscular
system (dantrolene) and (4) drugs active on the different systems (thiocolchico-
side). f3-blockers also reduce muscular hypertonicity of cervical spine, and they can
be employed as well as proper muscle relaxant drugs. Paracetamol could be com-
bined with myorelaxants such as tizanidine, a centrally acting α2 adrenergic ago-
nist, used 2–4 mg twice a day for 7/10 days. If dizziness or true vertigo is present,
this drug in not indicated due to its central effects on brainstem and thus on vestibu-
lar nuclei. In these cases, it is better to combine paracetamol with low doses of
benzodiazepines (BDZ) like diazepam 5 mg at night time.
In presence of nausea, it is possible to use metoclopramide 10 mg twice a day for
7/10 days. In these cases, L-sulpiride at low dosage (12.5 mg twice or three times a
day) also allows a good control of nausea and dizziness; it also has a mild myorelax-
ant action.
WAD is considered chronic if pre-accident activity levels are not gained within
6 months. Ongoing cervical pain and reduced range of motion (ROM) associated
with chronic WAD constitute both a prognostic and a therapeutic dilemma. The
location and severity of tissue injury and the prognosis of chronic neck pain may
depend on predisposing neck pathology. In addition to peripheral input, long-
standing neck pain (like other chronic pain conditions) may be associated with a
central component that can modify the pain threshold. Considerable research has
been dedicated to determine the direct and indirect roles of the zygapophyseal joints
in the generation of pain and dysfunction in whiplash injury [6].
Blocking the sensory nerves that innervate these joints reduced symptoms in
50 % of the subjects with chronic whiplash pain. However, this finding suggests that
no responders might have been suffering from a pathology related not to the joints
25 Pharmacological Treatment of Whiplash-Associated Disorders (WAD) 261
but to soft tissue. Almost nine of ten whiplash sufferers had some degree of muscle
spasm [7].
In particular, these patients had decreased ability to relax the trapezius muscles.
Such a finding raises the question of whether cervical muscular dysfunction causes
ongoing excess loading of the zygapophyseal joints, yielding the clinical picture of
chronic whiplash, or whether muscle dysfunction is an attempt by the body to splint
a subtly injured cervical spine.
Several theories about musculoskeletal pain syndromes such as WAD suggest
that pain and muscle activity interact and may contribute to the chronicity of symp-
toms. Studies using electromyography (EMG) have demonstrated abnormal muscle
activation patterns of the upper trapezius muscles in the chronic stage of WAD
(grade II) [8].
Concerning chronic treatment of whiplash-associated (WA) pain, the most com-
monly prescribed pharmacological agents are the same: oral muscle relaxants and
nonsteroidal anti-inflammatory drugs. Also in these cases, paracetamol has to be
preferred. However, the effectiveness of these drugs in chronic patients is limited by
their systemic therapeutic effect and unfavourable side effects. Physical interven-
tions such as mobilisation, manipulation and exercises have proved beneficial for
pain and dysfunction at least in the major part of the patients. Anyway, in chronic
WA pain, the only treatment that has clearly shown benefit is radiofrequency neu-
rotomy [9].
The potential benefits of relaxing selected neck muscles [10] with botulinum
toxin type-A (BTX-A) for the treatment of muscle pain in WA chronic head and/or
neck pain have been investigated by Freund et al. [11, 12].
BTX-A (Botox®) is a neurotoxin and is effective for treating a variety of disorders
of involuntary muscle contraction, including spasticity, cervical dystonia, blepharo-
spasm and hemifacial spasm. It inhibits neuromuscular signalling by blocking the
release of acetylcholine at the neuromuscular junction. The biological effects of the
toxin are transient with normal neuronal signalling returning within approximately
3–6 months postinjections. The injection technique used for the neck is based on
experience with cervical dystonia. The sites chosen are chiefly in the large superfi-
cial muscles, specifically, the splenius capitis, rectus capitis, semispinalis capitis
and trapezius. These muscles can easily be palpated in most individuals and can be
injected without sophisticated techniques. Most patients exhibit tender areas in the
larger muscles, often in conjunction with tight bands or knots. The neurotoxin
effects are thought to act only upon motor nerve endings, while sensory nerve fibres
are spared from such effects. Thus, analgesic effects are likely to occur, not as a
result of blocking afferent sensory fibres at the site of injection but rather from sec-
ondary effects that may be attributed to muscle paralysis, improved blood flow and
release of fibres under compression by abnormally contracting muscles. The pri-
mary action may affect alpha and gamma motoneuron function in the muscle spin-
dles resulting in lower muscle tone. BTX-A treatment is potentially a painful
procedure [13]. It is contraindicated in the presence of infection at the injection
site(s) and in individuals with known hypersensitivity to any ingredient in the for-
mulation. Individuals with peripheral motor neuropathic diseases or neuromuscular
functional disorders should receive BTX-A treatment with caution. BTX-A should
also be used with caution in patients receiving aminoglycosides or other agents
interfering with neuromuscular transmission.
BTX-A injections are not a curative treatment. BTX-A provides a temporary
paralytic effect and requires repeated injections to continue the beneficial effects.
The duration of effect is longer with the initial injection and progressively gets
shorter with repeated injections for most dystonic disorders. It is not known at this
time whether BTX-A can be readministered indefinitely or if the effectiveness will
wear off over time.
25.3 Whiplash-Associated Equilibrium Disturbances (WAED)
Whiplash injury is a very common cause of vertigo and dizziness. The physiopatho-
logical mechanisms of this kind of injury can be explained from the effect of forces
applied to the head and the neck during the collision. In the first phase, the force
applied to the rear end of the car during the collision results in a forward accelera-
tion of the body while the head is pushed backwards from inertial forces causing a
cervical hyperextension. In the second phase, which always occurs because of the
effect of inertial forces, the head is pushed forward with subsequent hyperflexion of
the neck. The whole duration of these phases is about 20 ms. This is the reason for
the lack of activation of neck neuromuscular protective reflexes, whose latency is
about 50 ms. During neck hyperextension the elongation of cervical rachidian tis-
sues may even reach 5 cm [14].
The vestibular system is frequently involved in whiplash injuries; lesions may
involve labyrinth and central vestibular organs and pathways.
Three lesion levels of the vestibular system can be distinguished: (1) labyrinth
and organ damage, (2) central vestibular and oculomotor system damage (3) and
both involvement of the peripheral and central vestibular systems. Table 25.1
reports the classification of post-traumatic vertigo (from [12], modified).
The prerequisites for successful pharmacological treatment of WAEDs are the ‘4
Ds’: correct diagnosis, correct drug, appropriate dosage and sufficient duration.
First, a correct diagnosis, on the basis of the patient history, clinical examination
and laboratory investigations; second, the correct drug—only a few have been
Table 25.1 Causes of post-traumatic vertigo

Damage site Lesions Physiopathology
Labyrinth Labyrinthine lesions, temporal bone Otolith displacement
fractures, concussive trauma, haemorrhagia
Maculae—semicircular canals Round—oval window rupture
Perilymphatic fistula
Vestibular nerve Axonotmesis neurotmesis Concussion—haemorrhage
Brainstem Concussion haemorrhage ischemia Neurotransmitter release
cerebellum
Cervical rachis Whiplash syndrome Vascular—proprioceptive
proven in controlled trials to be effective in a sufficiently large sample of patients,

but experience can suggest appropriate drug choice for every specific patient; third,
an appropriate dosage—often the initial dose is too low or too high so that the treat-
ment is either ineffective or not well tolerated; and fourth, a sufficient duration—
often drugs are either given for too long, such as antivertiginous agents (e.g.
dimenhydrinate), which delay central compensation and may cause drug depen-
dence, or not long enough.
In the child, pharmacological treatment of vestibular post-traumatic disorders is
essentially symptomatic for the early and efficient development of compensatory
mechanisms. The main aspects of treatment are related essentially to the dosages
and the frequency and duration of drug administration for each case. The choice of
substance is based on the clinical experience of the physician and on knowledge of
the pharmacological characteristics of the different categories of drugs [15].
In the elderly, pharmacological treatment of post-traumatic vertigo shows par-
ticular aspects linked to the aging processes. Several factors such as relative
enhancement of fat tissue, the reduction of body mass, decreased hepatic and kid-
ney functions and the diminution of serum albumin influence drug pharmacokinetic
properties (absorbency, tissue distribution, metabolism, sensibility and clearance).
We can distinguish therapies for vertigo spells, chronic unsteadiness or relapsing
vertigo.
25.4 Vertigo
Vestibular sedative drugs should be employed immediately after head-neck trauma

and continued for a few days.
In benign positional vertigo (BPV) drug treatment should principally support
rehabilitative training because neck pain and muscular stiffness and spasm make
difficult vestibular physical treatment in the early stage of the disease
Symptomatic therapy involves vestibular suppressor and antiemetic drugs.
Among the vestibular suppressor drugs, antihistamines, phenothiazines and benzo-
diazepines are the most widely used.
Antihistaminic drugs (dimenhydrinate, flunarizine, cinnarizine, hydroxyzine,
betahistine, astemizole) act on the synapses between the first and the second neu-
rons, on the reticular formation, on the vestibular dopaminergic pathways and on
H1 receptors. The pharmacological effect is vestibule suppressive with inhibition of
positional nystagmus.
Betahistine interferes with the diamine oxidase prolonging histamine action; it
has a moderate agonist activity on H1 receptors and a strong activity as an H3
antagonist. Betahistine inhibits neurons of the lateral vestibular nuclei [16] and
increases the basilar and cochlear flow in animal models. Betahistine has vasodila-
tative effects on stria vascularis, on spiral ligament and on vertebrobasilar circula-
tion [17]. Betahistine improves microcirculatory flow of the inner ear and central
vestibular system, and this can explain the positive effects in the treatment of parox-
ysmal peripheral vertigo, modulating effect on cerebral and labyrinthine circulation.
Astemizole has a strong inhibitory action on vertigo and nystagmus, and it is

interesting from a clinical point of view because it crosses the blood-cerebrospinal-
encephalic barrier only in a minimal concentration; for this reason this drug has
very low sedative effects, and therefore its main action is on the peripheral vestibu-
lar system [18].
Phenothiazines (promethazine, thiethylperazine, prochlorperazine) are very
effective in decreasing acute vertiginous symptoms and vegetative side effects.
Pharmacological effects on the vestibular system are the inhibition of peripheral
cholinergic inputs, inhibition of H1 receptors in vestibular nuclei and an effect on
the bulbar chemoreceptor trigger zone. Phenothiazines have important side effects
on the extra pyramidal system, on pressure control mechanisms and on prolactin
secretion. For these reasons phenothiazines should be administrated carefully espe-
cially in the elderly.
Scopolamine shows strong anticholinergic activity on brainstem, reticular for-
mation and vestibular nuclei. This drug cannot be used in patients suffering from
glaucoma, prostatic hypertrophy and heart diseases [19–21].
Benzodiazepines (diazepam, lorazepam, clonazepam, etc.) enhance GABAergic
inhibitory properties of vestibulocerebellum on vestibular nuclei and activate the
internuclear inhibitory pathways. They are also active on glycinergic pathways, on
substantia nigra, on the limbic system and on cholinergic activatory reticular forma-
tion. The final effect is the inhibition of the vestibulo-oculomotor reflex and nystag-
mus. Benzodiazepines have inhibitory effects on breathing and blood circulation
and for these reasons should be carefully administered in elderly patients.
Propranolol has been successfully employed in the treatment of whiplash injury-
related vertigo. This drug reduces hypertonicity of spinal muscles lowering the dis-
charge frequency of neuromuscular
fusicellular endings, with a subsequent diminution of cervical pain [22].
25.5 Chronic Unsteadiness and Relapsing Vertigo
Damage to the vestibular apparatus due to whiplash injuries produces acute symp-
toms, which gradually improve as central compensation occurs. The aim of the
pharmacological strategy in peripheral vestibular lesions is to improve CNS restor-
age mechanisms; for this reason vestibulo-suppressive drugs, even if effective in
reducing vertigo and imbalance, worsen the CNS compensation and should be
administered only in the first stage of the disease. On the other hand with the
employment of CNS excitatory drugs or drugs with decompensating effects during
rehabilitative training, compensation processes will be stimulated with acceleration
of healing.
Among drugs which enhance compensation processes, the amphetamines,
ginkgo biloba and calcium antagonists are the most used [23–25]. Amphetamines
theoretically could be employed in the treatment of peripheral vestibular lesions
based on their positive effects on compensation processes. Their use is limited
because of significant side effects. Pemoline and fipexide belong to this category of
Table 25.2 Neuroactive drugs not specifically acting on vestibular neurotransmitters

Metabolic enhancers Citicoline, deanol, piracetam, oxiracetam, ginkgo biloba,
protirelin, l-acetylcarnitine
Neurotrophics Gangliosides
Excitants Amphetamines, fipexide, pemoline
Antidepressants Tricycles IMAO, sulpiride
Anticonvulsants Carbamazepine
Myorelaxants β-blockers Baclofen
Table 25.3 Neuroactive drugs specifically acting on vestibular neurotransmitters

Antihistamines Flunarizine, cinnarizine, hydroxyzine, astemizole, betahistine,
diphenhydramine, dimenhydrinate
Phenothiazines Promethazine, thiethylperazine, prochlorperazine
Benzodiazepines
Scopolamine
drugs and are particularly interesting for their limited side effects; pemoline affects
dopamine turnover and has few peripheral effects; fipexide affects the reticular for-
mation and shows dopamine-like effects. Ginkgo biloba enhances postural and
locomotor balance and oculomotor function recovery in experimental unilateral
vestibular lesions.
Cinnarizine and flunarizine [26] selectively block calcium entry into peripheral
vestibular system cells (especially cristae cells); both these drugs show antihista-
minic and anticholinergic activities. In the peripheral vestibular system, calcium
antagonists modulate neurotransmitter release. Flunarizine interferes in ACh release
and enhances compensation processes. In elderly patients, these drugs should be
administered carefully for its Parkinson’s-like effects after prolonged treatment [27].
In the elderly where CNS reorganisation after vestibular damage is less effective,
drugs with positive effects on compensation, as well as haemorrheologic and neu-
roactive drugs, should be used. Drugs which increase CNS neurotransmitter storage
will be also useful in these patients [28]. In particular, neuroactive drugs are
employed for their actions on CNS neurotransmitters, while vasoactive substances
improving blood macro- and microcirculation enhance CNS metabolism.
Neuroactive substances can be classified as drugs not specifically acting on vestibu-
lar neurotransmitters and drugs specifically acting on vestibular neurotransmitters
(Tables 25.2 and 25.3).
Among the neuroactive drugs which are not specifically active on vestibular neu-
rotransmitters, citicoline has dopaminergic and serotonergic activities and reduces
platelet aggregability. Deanol and oxiracetam have cholinergic action; piracetam, a
GABA derivative, has strong dopaminergic and mild GABAergic activities and
improves cerebral ATP synthesis; this drug accelerates compensation phenomena
and is well indicated in vertigo due to a brainstem disinhibition [29] and in post-
traumatic vestibular lesions. Protirelin is a TRH derivative; this drug’s main effect
is on the cholinergic neurotransmitter system and it shows secondary effects on the
dopaminergic, noradrenergic and serotonergic systems.
Among alpha-blockers, dihydroergotoxine, an alkaloid derivative, has vascular

and metabolic activities enhancing alpha-adrenoceptor blocking activity.
Dihydroergotoxine also has a dopaminergic activity and inhibits the specific cere-
bral phosphodiesterase response in c-AMP metabolism. Their use is however lim-
ited to selected cases. Nicergoline is an ergot derivative with actions on dopamine
turnover, on cerebral blood flow and on cerebral glucose consumption; this drug
enhances neurotransmitter storage, and for this reason its employment seems to be
interesting in post-traumatic vertigo of central origin especially in the elderly.
Drugs active on the microcirculatory system have been found to have multiple
actions on the neurotransmitter system, on cerebral flow and on cerebral metabo-
lism with limited side effects. Among these substances buflomedil [30] has alpha-
blocking, antiaggregant and haemorrheologic properties and a calcium antagonist
effect. This drug acts to diminish cerebral oxygen consumption. Pentoxifylline has
different pharmacological properties; the main one is the improvement of erythro-
cyte deformability (through an ATP improvement) and the diminution of blood vis-
cosity (through a diminution of fibrinogen). This drug reduces platelet aggregation
by acting on membrane phosphodiesterases, reducing thromboxane synthesis and
improving at the same time the synthesis of prostacyclin. Pentoxifylline reduces
platelet adhesiveness to the vessel wall and results in delaying the thrombogenic
action. Among calcium antagonists, nimodipine improves dopa’s inhibiting action.
In chronic WAD, paying attention to the patient’s age and the metabolism [31],
cinnarizine and flunarizine may be used, at the lowest dosage possible and for the
shortest possible period. Cinnarizine has vasodilatatory, antihistamine and anticho-
linergic effects inhibiting central vestibular system activities. The main CNS action
of flunarizine, difluorinated derivative of cinnarizine, is blocking Ca2+’s entry into
cells during hypoxia.
Sometimes post-whiplash headache, generally a tension-type headache, in pre-
whiplash migrainous patients may evolve into the vestibular migraine. Characteristic
features include recurrent attacks of various combinations of vertigo, ataxia of
stance and gait, photophobia and phonophobia and other brainstem symptoms,
accompanied or followed by head pressure, pain, nausea or vomiting [31]. Tricyclic
antidepressants in combination with diet gave a good response. Generally, only
drugs that are effective for treating migraine with and without aura can currently be
recommended. For the therapy of acute attacks, aspirin and an antiemetic could be
offered, whereas metoprolol (100 mg/day), topiramate (50–100 mg/day) or valproic
acid (300–900 mg/day) could be offered for prophylaxis.
Very rarely, and only after a major and complex whiplash such as rear and con-
sequently front collision, atlantooccipital strain may lead to a central vestibular
lesion inducing downbeat nystagmus (DBN, a form of acquired nystagmus that is
characterised by slow upward drifts with downward quick phases). Patients fre-
quently report blurred vision or oscillopsia, which increases on lateral gaze, as well
as associated unsteadiness of gait and postural imbalance. As a pathophysiological
mechanism, a tone imbalance of the central vestibular pathways subserving vertical
eye movements, including the otolithic pathways, such that DBN is often gravity
dependent, has been proposed for DBN. Baclofen and clonazepam dosage of 0.5 mg
tid or 1 mg bid, both GABA agonists, improve DBN [32].
Pharmacological therapy can be employed during rehabilitative treatment. The

aim of drug treatment is to reduce hypertonic contracture of muscles of the neck
to facilitate physiotherapeutic treatment and to improve the efficacy of such ther-
apy. In these cases, muscle relaxant substances may be employed. Also drugs
acting on central plasticity mechanisms may be useful (e.g. piracetam).
Amantadine results to be particularly useful in WA chronic unsteadiness espe-
cially when it is due to a labyrinthine damage. Amantadine [33–35] on one hand
reduces vestibular organ damage through an anti-glutamate action on NMDA
labyrinth receptors and on the other hand through dopaminergic mechanism
improves compensation.
In labyrinthine post-traumatic lesions (direct or indirect through labyrinth con-
cussion or vertebral artery spasm), the preferred drugs are those with positive effects
on vestibular compensation. Vestibular suppressive drugs would be helpful initially
to improve vertigo and neurovegetative phenomena but should be avoided for long
treatments.
In post-traumatic vertigo of central origin (generally caused by vertebrobasilar
acute insufficiency), drugs which are active on neurotransmitter systems may be
employed together with vasoactive substances improving CNS circulation and
metabolism. In the brainstem involvement, drugs which are active on the cholinergic,
histaminergic and adrenergic neurotransmitter systems (scopolamine, cinnarizine)
are effective in reducing symptoms but can interfere with the processes of compensa-
tion. In cases exhibiting lack of cerebellovestibular control, drugs with GABAergic
actions such as benzodiazepines may be employed successfully [30, 31].
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Physiotherapy of Neck, Back and Pelvis
26
I. Odkvist, L.M. Odkvist, S. Negrini, and C. Mariconda
26.1 Introduction
Recent studies highlight the fact that where there is pain in a WAD patient, there is
a rapid alteration of neck muscle functioning. It has been seen that within 24 h of
the trauma, there is an alteration in muscle control: on the contrary, there is no
proof of an automatic recovery if the pain diminishes and so special training is
necessary [1, 2].
Physical exercise plays a major role in rehabilitating the patient, integrating him
back to a normal life. It is possible to identify some goals to be obtained in WAD
rehab:
1. Activation of the deep neck muscles (exercises with a low load)
2. Re-education of deep neck muscle resistance
3. Realignment of the activation patterns of both the deep and the superficial neck
muscles
4. Posture realignment, also during functional tasks
5. Readjustment of force and resistance to functional necessities (exercises with a
high load)
The basic principles of physical exercises are the segmentation, simplification
and an increasing and continuous feedback. This treatment is executed with the
patient in various positions, from the supine up to the orthostatic, so as to pass from
a low workload to a more elevated one.
I. Odkvist • L.M. Odkvist

Physiotherapy, Risbrinksgatan 6a, Linkoping, Sweden
Department of Otolaryngology, University Hospital, Linkoping, Sweden
S. Negrini (*)
Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy
e-mail: stefano.negrini@med.unibs.it
C. Mariconda
Department of Physical Medicine and Rehabilitation, Gradenigo Hospital, Torino, Italy

270 I. Odkvist et al.
The motor control of the scapular girdle must not be overlooked seeing that a
variation of load distribution on the spine will negatively increase the compressive
load on the cervix vertebrae.
Scientific evidence [3] has been collected for a multimodal programme which
foresees:
– Explanations and reassurance for the patient
– Encouragement in activities and movement
– Pain relief
– Therapeutic exercises
– Ergonomic strategies
26.2 Orthopaedic Collar
Keeping in mind the numerous clinical variables and subjective ones of WAD, more
recent new studies highlight the importance and long-term efficacy of a swift mobil-
isation and treatment of the symptoms of distortion trauma. The mobilisation is
carried out in terms of treatment and pain prevention of the disability and conse-
quent recuperation of good specific muscle control.
In some cases we have noticed that immobilisation, where not clinically ade-
quate, even if followed by rehabilitation treatment has led to a longer recovery time
and longer absences from work. This also evidently means an increase in health and
social welfare costs.
26.2.1 Physiotherapy
Decontraction is usually the very first step. It can be achieved by relaxing the patient,
letting him feel confident with the therapist. This is easier, for example, in a good
environment, as happens in water, but for everybody it is suggested to work gradu-
ally, with the head well fixed at the beginning resting on the table and then in the
therapist’s hands with a very good manual grasp. Many exercise techniques able to
reduce pain do exist and can be used in conjunction with decontracting and strength-
ening manoeuvres when one begins to remove the collar. We can mention, for
example, the McKenzie method [4], the Mézières, Souchard or Bienfait approaches,
the Sohier or Maitland technique, and so on. Obviously, The Method does not exist,
but only many useful techniques that must fit the pathology of a single patient and
the knowledge and ability of the physiotherapist. Physiotherapy is not only muscu-
lar (and psychological) relaxation: it is also a first step in returning a part of the body
to its normal daily life activities. This means that exteroception and proprioception
play a role other than the simple goal of decontraction.
The evidence suggests that physical exercises [5, 6] may be beneficial in the
short and long term. According to our experience, regaining enough strength to
permit not only movement but usually also the ability to sustain the head is perhaps
the most important goal when rehabilitation begins. In fact, the collar reduces
26 Physiotherapy of Neck, Back and Pelvis 271
muscular usage, provoking deactivation that combines with injury and pain to
reduce strength and trophism of muscular tissue. The early stage of rehabilitation
constitutes also a very important step in regaining proprioceptive input from the
muscular and articular tissues.
There are some techniques that are fundamental and cannot be ignored during
early stage of treatment: isometric strengthening and rhythmic stabilisation. The
first one constitutes a type of contraction more than a real technique and must be
done at the beginning in a neutral position along the classical axes of movement and
then at different degrees of movement as well as the intermediate plane. This is very
important because the muscular tonic fibres are prevalent in the neck musculature
due to its physiological role and because the first step is to permit the head to be
stable over its “slender column”.
The second technique involves movements effectuated by the patient with the
opposition of the therapist, provoking isometric and eccentric contractions along
different axes of movement. This technique greatly increases both the strength and
also the proprioceptive input. Having gained strength it is then necessary to gain
mobility too. As we saw, it is possible to recover both together, but it is also wise to
include in a good programme exercises along all the axes of movement, not ignor-
ing the protraction-retraction movement. These exercises at the beginning will be
passive and conducted by the therapist while respecting the pain. As both the patient
and the therapist will become more confident, pain will be explored more, particu-
larly using active (assisted or not) contraction to avoid overstretching. Active exer-
cises are very useful at this stage, and also auto-mobilisation can be applied. The
literature suggests that these techniques can be used as an adjunct to strategies that
promote activation and that they can be beneficial particularly in the short term.
There are techniques developed to “normalise” the joint positions. These can be
more or less gentle, depending on the method. They are an important way to regain
good joint positioning, normalising in this way the afferents, reducing muscular
hypercontraction and avoiding pain. Studies about these techniques have not been
published. As has been sufficiently stressed above, proprioception plays a funda-
mental role in all the rehabilitation programmes, permitting good range of move-
ments once it is possible. We do not think that neurology is the key to open the door
of orthopaedic rehabilitation, as others involved in rehabilitation have proposed, but
we are conscious of the importance of not neglecting this fundamental element.
The literature does not address postural control improvement as a single thera-
peutic element; rather, many researchers have proposed it as a part of a multimodal
treatment plan.
It is not possible to only propose a cervical intervention, because the neck has a
function: let the eyes look forward. This function must be accomplished indepen-
dently by the various elements, and this means based on the posture of the rest of
the body. This posture must be compensated by the neck. This is why it is of enor-
mous importance to intervene and modify the posture of the body if we want to
prevent other stresses on the neck. When rehabilitating a neck it is not possible to
neglect the other parts of the spine. The vertebral column in fact has been defined as
one articulated long bone, and an injury in one part always reflects on the other
(apart from a lesion developed during the injury itself). This is why it is very
important to consider the thoracic and lumbar regions too.
Active participation of the patient is a cornerstone of effective physical treat-
ment. Therapists used to think that a patient must rely on them and that without their
help the patient will not be able to work properly. Perhaps this is true, but what is
much more important is what the patient loses by not working on his own. Working
at home is fundamental, and particularly isometric exercises and the ones necessary
to regain mobility can be done and controlled without many problems.
26.2.2 High-Frequency Proprioceptive Reprogramming
High-frequency proprioceptive reprogramming (HFPR) [7] permits intervention at

an archeo-proprioceptive level, which means all the impulses sent from the periph-
eral structures which reach the subcortical processing structures (spinal cord, ence-
phalic trunk and cerebellum). This instrument activates a series of stimulations
which are much more complex than those perceived during a simple exercise on a
self-stabilising board. The HFPR (Delos®) signifies a self-stabilising board having
one or two degrees of leeway and being connected to a PC allowing monitor visuali-
sation of the exercises with visual feedback (Fig. 26.1).
The patient has to govern a series of high-frequency proprioceptive stimulations
in diverse situations of unbalance which force him to activate his archeo-
proprioception to the most with particular attention to the spinal proprioceptive
reflexes. These reflexes are the base of a correct functional stability of the joints.
Postural command also receives benefit from proprioceptive training seeing that its
quality (above all in dynamic situations) is based on the synergic action of archeo-
proprioception, sight and the vestibular system. It is absolutely fundamental to cre-
ate situations of disequilibrium in a monopodalic position on a self-balancing board
having visual feedback to obtain an exact assessment of disequilibrium control.
26.3 Neuromuscular Taping
Neuromuscular taping (NMT) [8] is a rehabilitation system using elastic self-

adhesive tape applied to the skin. It functions locally and at a certain distance
through reflexes as it stimulates both the deep and superficial skin receptors through
body movement by sending exteroceptive and proprioceptive stimuli to the central
nervous system which generates a muscular reflex reaction.
The tape is made of water-resistant cotton which is elastic lengthwise and pro-
vides 40 % extra elasticity to the skin.
The two principal application techniques of the NMT are decompressive and
compressive mode.
In both cases the effect is aimed at the vascular, lymphatic, skin, muscular and
nervous structures and is used for the subsequent rehabilitative goals:
– Pain reduction
– Implementation of local vascularisation through reabsorption of oedemas and
haematomas
Fig. 26.1 Delos® equipment.

Subject stands on the board
with one or 2 ft and tries to
maintain equilibrium. Body
and board sway are
contemporary recorded and
presented as visual feedback
in order to improve visual
control of dynamic posture
stabilisation
– Normalisation of muscular tone

– Joint realignment
– Postural improvement
Even if there is no scientific evidence of the above article, neuromodulative
activity of pain impulses from the posterior horns of the spinal cord can be hypoth-
esised. Neuromuscular taping is therefore a valid and efficient rehabilitative instru-
ment to be integrated into WAD diagnoses, both in acute, post-acute and chronic
phases.
26.3.1 Physical Therapy
The main goal of physical therapy is to promote soft tissue healing and to diminish
inflammation. Few studies in literature investigated the effect of physical therapies
in treating patients with whiplash-associated disorders (WAD), and their efficacy
has not been demonstrated in this group of patients [9].
26.3.1.1 Heat
Many times heat has to be proscribed in the cervical region, and this is particularly true
in whiplash injury: the sympathetic plexus is placed around the vertebral artery and can
be influenced by this type of treatment with dangerous effect, particularly when a lesion
is suspected here. Vertigo can commonly appear using heat in the cervical region, and
that is why, when vertigo is a major complaint, it is better not to try this type of therapy.
Infrared is very superficial and could be used, with some cautions, associated with mas-
sage. Radar therapy and Marconi rays are forbidden because of the heat that develops,
as is the case for ultrasound therapy, which could micromassage the soft tissues.
26.3.1.2 Cold
This type of therapy does not have a great significance and is not usually used in
such cases.
26.3.2 Mechanical Therapy
The most important danger in treating whiplash is excessive mobilisation of a struc-

ture not completely repaired. This is what could happen with all manual therapies,
and this is why it is necessary to be very cautious, particularly if the healing process
could not be completed.
Manipulation is a common treatment but its value has not been established till now.
According to our experience it is inappropriate in whiplash patients, because it is pos-
sible to obtain mobility and a pain-free situation with less risks using simple exercises.
Massage can be applied, but it must be relaxing to reduce muscular contraction
particularly just before and after physical exercise therapy.
Traction. There is only one study [9] addressing the problem of traction of patho-
logical necks, but it did not focus on whiplash and its results were not definitive.
The most important danger with this treatment is the damage to soft tissues, with
overstretching of ligaments, capsule of zygo-apophyseal joints and (less important)
muscles. This is always present to a lesser or greater degree, and this is why trac-
tion, according to our thought, must not be applied.
26.3.3 Electrotherapy
This type of therapy is not so useful. Transcutaneous electrical nerve stimulation

(TENS) can reduce pain; iontophoresis can have an anti-inflammatory effect, but
their importance is not very great in whiplash injured patients.
26.3.4 Laser Therapy
It can be useful if trigger points can be detected. Particularly useful, in our

experience, are the He-Ne and the As-Ga lasers.
26.3.5 Magnetotherapy
There are results in the literature [9] about the association between the use of a
collar and continued magnetotherapy with benefits in the short term. In our experi-
ence, it is possible to prescribe a 20-min application for at least 20 times: usually it
is necessary to use 60 G with a frequency of five times a week.
There are only two controlled trials that examined the efficacy of pulsed electro-
magnetic treatment (PEMT) in the treatment of patients with acute WAD. The study
of Foley-Nolan et al. [10] compared PEMF treatment versus sham PEMF treatment.
The authors found that PEMF treatment significantly reduced pain after 4 weeks
compared with sham treatment, but not after 3 months. Similarly, Thuile and Walzl
[11] showed a significant reduction in pain and improvement in cervical ROM in
patients treated with PEMT compared with those who received medication alone.
Although there is some evidence that PEMT decreases pain intensity and increases
cervical ROM over the short term, the evidence is insufficient to support the use of
this treatment with confidence.
Heat, ice, massage, transcutaneous electrical nerve stimulation (TENS), pulsed
electromagnetic treatment (PEMT), electrical stimulation, ultrasound, laser and
shortwave diathermy may be prescribed for the treatment of Grades II and III WAD
as optional adjuncts to manual and physical therapies and exercise.
26.3.6 Acupuncture
While this technique is not recommended for Quebec Grade I WAD, it can be
employed in Grades II and III WAD as an optional adjunct for symptoms lasting
more than 3 weeks.
See also chapters 36 and 37
Regarding laser acupuncture one controlled trial investigated the efficacy of
laser acupuncture combined with cervical collar use versus treatment with collar
and placebo laser [12], but this technique does not appear to be any more effective
than the placebo in treating acute WAD.
26.4 CARET Therapy
The acronym CARET indicates capacitive and resistive energy transfer. This inno-
vative rehabilitation instrument utilises the transmission of long waves within bio-
logical tissues consequently stimulating energy production in the tissues and
activating repair and anti-inflammatory processes at a cellular level. The physiolog-
ical effects confirming the energy transfer are:
– Reduction of the viscosity of connective tissue with a consequent increase in
extensibility
– Vasodilatation with local increase in blood flow and a consequent removal of
algogenic substances
– Drainage and resorption of oedemas and haematomas, resorption of excess

synovial fluid
– Reduction of muscular spasms owing to reduced activity of secondary efferents
– Repair of fibril muscle damage
– Reintegration of membrane potential in nerve fibres
In processing the WAD results, we find indication both for pain control and
reparative scopes, therefore permitting a better clinical response and a reduction in
recovery time.
26.4.1 Treatment Planning
A collision victim becomes hypervigilant for any symptoms that before the colli-
sion might have been disregarded but because of amplification became far more
intrusive. The symptom pool may increase even though the acute injury is resolving.
These initially minor symptoms may be due to occupation, sports or hobbies, symp-
toms from medication use and importantly attributable to maladaptive postures and
changes in physical fitness that arise as patients withdraw from normal activities.
These various benign, physical sources do not usually cause severe or significant
pain but this is where psychological factors begin to become important.
In the acute stage painkillers and anti-inflammatory drugs like nonsteroidal anti-
inflammatory drug (NSAID) for the first 2 weeks may be given, and this can be
combined with paracetamol. The physiotherapist, in the first 24 h, can use cold
packs to prevent pain, unnecessary tissue swelling and oedema. A soft, supporting
cervical collar should be used the first few days after injury. The collar offers sup-
port for the neck and head in a pain-free position with the neck in a favourable posi-
tion. After a few days the collar should be taken off a number of times each day.
During these hours the neck is trained with gradually increasing active exercises. It
is important to know that the recovery is not delayed by not using the collar. Short
periods of collar use are suggested by some authors [13]. The patient should avoid
excessive use of the collar, which could cause bad posture and delay mobilisation.
The collar may also be suitable for nocturnal use. The patient should avoid sleeping
on the stomach as this causes an extreme extension and sometimes rotation of the
cervical spine.
For sleeping a suitable pillow is advisable, offering support to the head with the
head in a median position and the cervical muscles relaxed.
In the acute phase acupuncture has its role for pain relief starting carefully as
soon as possible after the accident and increasing in intensity and number of needles
as days go by. Massage may be tried.
In the subacute phase, after approximately 2 weeks, more active physiotherapy
can be given. The physiotherapist performs a new examination concerning the
range of movement and the muscular status. Mobilisation is instructed and per-
formed with care, first free active movements and later turning, leaning and flexion
movements against the resistance of the hand of the therapist. Biofeedback training
is helpful. This induces muscle strengthening enabling the patient to cease using the
collar.
Now is also the time for treatment of other parts of the body. Thus the physician
and the physiotherapist have to examine the range of movement in the cervical,
thoracic and even the lumbar parts of the spine, as thoracic and lumbar disturbances
are common in traffic accidents together with neck lesions.
Hypermobility and hypomobility are looked for. Asymmetries are noted.
Hypermobility is usually most common in the lumbar back, caused by traffic
trauma. Muscular stabilisation training is instructed and is usually the only treat-
ment necessary.
Hypomobility is most common in the thoracic spine. The treatment is vertebral
joint mobilisation.
In this stage it is of uttermost importance to induce leg muscle strength training,
as for balance, walking and returning to a normal life the use of the legs for appro-
priate stance and body support is mandatory. For the patients self-confidence, one
basic thing is the possibility to move around freely and be able with muscle power
to counteract imbalances and not have to stop walking or training due to lack of leg
muscle ability.
The sacroiliac joints are very important to examine after traffic accidents. The
symptoms may be obscure and delayed in appearance. Sometimes symptoms and signs
appear years after the trauma. The patient is examined standing up. Differences in
height between the right and left iliac crests are looked for. The Vorlauf phenomenon,
when one spina iliaca posterior is immobile when the patient bends forward, indicates
immobility in one sacroiliac joint. The patient is treated according to the findings, with
mobilisation of the immobile joint. This is performed with the patient in a lateral or
prone position, the sacrum fixed and the iliac bone mobilised by the physiotherapist.
Massage may help some patients considerably but in others increase the pain.
In the subchronic and chronic stage, more stabilisation training is performed,
including neck movements with muscle strengthening. The training is performed,
supervised and instructed by the physiotherapist and also with a written home train-
ing programme. Video instructions are advisable. Both for neck training and general
robustness of the whole body, training in water is of benefit.
Most whiplash patients have balance problems caused by a brainstem distur-
bance or being of neck origin – cervical vertigo [14, 15]. Neck treatment may help,
but often true balance training is needed: walking, turning, head and eye movements
and standing on one leg, on a hubcap or on foam rubber [16, 17]. The automated
training in the computerised force plate, the Balance Master, is of great help. The
trauma may have caused benign positional paroxysmal vertigo, which craves a spe-
cific treatment [18].
The patient may be very tired and also have mental problems, with fatigue and
depressive tendencies. Hence the psychological approach has to be considered by
all members of the treating team, especially the physiotherapist who has a lot of
contact with the patient, repeatedly and often in long sessions. The goal is to help
the patient return to a normal family life and also to work.
26.4.2 Follow-Up
For the subsequent weeks, months and even years, it is of importance to have a well
programmed follow-up of the whiplash patient. This should preferably be per-
formed by the initial treatment team, who knows the patient and has participated in
the assessment. The follow-up takes into consideration all angles of the problems,
the neck, back, pelvis and balance, as well as the psychological and practical prob-
lems. The treatment results are recorded by case history according to a question-
naire and clinical investigation including balance testing. Stabilometry or, even
better, dynamic posturography is performed for an objective assessment of the defi-
cit and improvement in balancing ability.
26.5 Education or Advice
Numerous studies include education [19] or advice as components of the interven-

tion using educational videos and pamphlets. Ferrari et al. [4] found no beneficial
effect of a one-page pamphlet of evidence-based whiplash prevention information
on patient perceived recovery at 2 weeks or 3 months. Pamphlets emphasising the
good prognosis of whiplash were distributed to all participants in the Kongsted
et al. [20] trial, which found no clinically meaningful differences between rigid col-
lar, usual care with an emphasis on fear reduction and resuming normal activities,
and active mobilisation at 1 year.
By contrast, educational videos were shown to have beneficial effects on
improvement in pain among acute whiplash patients. They received by mail the
20-min video that provided reassurance, home exercises and advice on early return
to normal activities or watched from their bedside a 12-min psycho-educational
video emphasising behavioural and home exercise interventions and breathing
relaxation for muscle tension. In subjects there was relief from pain at 1, 3 and
6 months after injury, and they also used much less medication and had lower rates
of health-care utilisation [21].
Conclusions
Patients that normally receive conservative interventions are those with Grades 1
and 2 WAD. Conservative treatment includes local heat and ice treatment, neck
collar immobilisation, ultrasound, traction, massage, (active) mobilisation, exer-
cises, pulsed electromagnetic therapy and multimodal rehabilitation.
Active interventions that stimulate the patient to return to daily activities as
soon as possible are preferable to rest and wearing of a collar.
Physical therapy specifically aimed at the musculature (e.g. transcutaneous
electrical nerve stimulation, ultrasound, heat, ice and acupuncture) improves
prognosis in acute WAD.
In chronic WAD, the only treatment that has clearly shown benefit is
radiofrequency neurotomy [2].
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Manual Medicine in Whiplash-
Associated Disorders (WAD) 27
G. Brugnoni, C. Correggia, and C. Mariconda
27.1 Introduction
Manual Medicine (MM) is a medical discipline devoted to diagnosis and

conservative therapy of some algetic pathologies of the muscular-skeletal appara-
tus and in particular the rachis: such consequences are benign but extremely
widespread.
In the beginning MM availed itself of numerous techniques from American oste-
opathy, an alternative medicine [1], which had the undeniable merit of drawing
attention to the micro-mechanical problems of the rachis which had been unrecog-
nized by traditional medicine, even if these had been considered as the cause or
possible co-cause of all diseases. Osteopathy was, and still is, based on obsolete
scientific conceptions and is lacking in simple and clear diagnosis repeatable by all
operators seeing as it is based on deep palpation of fine intervertebral movements.
Benign vertebral pain reported in the majority of cases is more often linked to a
dysfunction of neuro-motorial control of the rachis [2] and not always owing to a
lesion.
A step forward was made by R. Maigne [3], through the conception of new
simple and repeatable semeiotics [4, 5] based on pain-provoking manoeuvres with
the aim of identifying pain in one or more mobile vertebral segments. In the absence
of organic lesions, Maigne defined this situation as “painful minor intervertebral
dysfunction” (PMID), an excellent definition for the majority of vertebral
dysfunctional pathologies.
G. Brugnoni
C. Correggia • C. Mariconda (*)
Department of Physical Medicine and Rehabilitation, Gradenigo Hospital, Turin, Italy

282 G. Brugnoni et al.
Research began by the Audiology Clinic of the University of Milan at the end of
the 1990s to use the diagnosis and manipulative techniques of MM for Ménière’s
disease [6] and then in other vertiginous pathologies, above all those of vertebral
origin.
The dysfunction of neuro-motorial control and consequent alterations of the neu-
romuscular patterns of the rachis, in problems of equilibrium, can cause a dysfunc-
tion to the vestibule-vertebral unit (see Chap. 7), that is, the anatomic-physiologic
structure which controls the connections between the proprioceptive trigeminal and
cervical-dorsal information and the neurovegetative ocular and labyrinthic
regulation.
27.2 Diagnosis
The clinical examination proposed can be divided into six principal parts:
1. Static examination of the rachis, of the head and limbs in an upright position
paying visual attention to the anatomic elements concerning modifications of the
physiological or pathological curves of the rachis and the position of the head,
shoulders and hips.
2. Dynamic examination of “segment” movements, to identify limitation of move-
ment, point of pain occurrence during circular movement, abnormalities during
harmonious movements and the rigid tracts of the spine or deviations from the
movement plan noted during bending and lateral-bending movement.
3. Examination of mobile vertebral – segments comprising a series of provocative
manoeuvres to provoke pain in the “mobile segment”, that is, the intervertebral
articulation, in the entire rachis, in a caudal sense from C6 to L5, searching for
one or more painful mobile segments:
• Axial pressure on the spinous processes
• Lateral pressure on the spinous processes
• Pressure on the first supraspinous and interspinous segment
• Search for the paramedian articular pain point
4. Examination of the cutaneous, subcutaneous, sinuous, periosteal and muscular
tissues, that is, of the “myofascial” pain. R. Maigne described a series of signs
visible at the cutaneous, subcutaneous, fasciae, tendons, periosteum and muscu-
lar levels which he called “cellulo-periosteo-myalgic syndrome”.
5. Examinations of neurological signs and of the pachymeninx
The description of a complete neurological examination is beyond our topic,
but it should be systemically carried out in WI and is extremely important for
decisions about instrumental exams and therapeutic choices.
6. Pre-manipulation tests
The following are absolutely necessary before proceeding with cervical
manipulation:
• Romberg, sensitized by rotation and extension of the head
• Localization of the spontaneous and positional nystagmus mainly by rotation
and extension of the head
27 Manual Medicine in Whiplash-Associated Disorders (WAD) 283
• Rancurel test for haemodynamic vertebral basilar insufficiency

• Positioning and cautious tensioning in cervical rotations assessing the
patient’s sensations
27.3 Treatment
Modern MM employs various manual techniques including both active and passive
mobilization, J. Mennel’s joint play, manual traction, transverse and longitudinal mus-
cle stretching and Mitchell’s post-isometric techniques as well as “vertebral manipula-
tion” differencing from the aforementioned in the way it is done and the type of sensorial
and proprioceptive stimulation, aiming at a major impact and rapidity of action.
Alongside the above methods all the modern antalgic techniques are used in
MM, such as articular, vertebral and peridural infiltrations, mini-invasive tech-
niques, instrumental and rehabilitative therapies amongst which the recent spinal
stabilization through biofeedback [7, 8] and Natchev’s vertebral auto-traction [9].
27.3.1 Manual Therapy
All “soft tissues”, skin, subcutaneous, fasciae, periosteum and muscles are obvi-
ously an integral part of the movement apparatus, both because they move together
with bone segments, that is, by accompanying movement – in the case of muscles
they are the engine – and because they are closely connected to the rachis for the
metameric distribution of the somatic and sympathetic innervation, and also, even
if in a less clear way, they are connected to extra-vertebral articulations.
Thus, for different reasons, but mainly for the achievement of a good clinical
result, it is necessary to be able to use these techniques correctly. They are extremely
useful both as a gradual preparation for manipulation or as a substitute when manip-
ulation is not possible owing to general or topical causes. These techniques can also
be employed to eliminate problems which persist after manipulation and which
could impede a quicker functional recovery.
As we have already mentioned, manual techniques can be subdivided into vari-
ous chapters, but those with more interest for us can be gathered into three groups:
27.3.1.1 Articular Techniques

To perform a mobilization of intervertebral and peripheric articulations.
1. Passive articular mobilization following the direction of active joint movements.
These are part of traditional kinesiatrics together with active or active-assisted
mobilization.
2. “Joint play” by J. Mennel [10], passive articular mobilization using lateral or
sliding movements which the articulation is not able to do actively.
3. Post-isometric relaxation (PIR) by Mitchell [11] or post-isometric release.
This technique entails guiding the two articular extremities to their maxi-
mum excursion, i.e. in tension, in a state of maximum release; then the therapist
asks the patient to move in the opposite direction against a minimum resistance
provided by the therapist for a duration of about 10–30 s: the therapist then
moves the articulation back to a maximum excursion and repeats this 3–5 times.
4. Inhibition of the antagonist. Requires isometric contraction against a minimum
resistance and then passively move the articulation in the same direction.
5. Inhibition of the agonist, who is asked to contract isometrically against a mini-
mum resistance and then move the articulation passively in the opposite direc-
tion. These techniques utilize the two laws of Sherrington such as the Kabat
method but without using maximum contractions.
27.3.1.2 Muscular Techniques

The aim is to release muscles which are prone to local contractions which may vary
in degree. The most efficient techniques are those which utilize stretching through
passive articular movement preceded by an agonist or antagonist’s contraction
according to what is expounded above. These movements must be associated with
manual transversal or longitudinal stretching and to techniques to facilitate the
neuro-motorial response.
27.3.1.3 Skin and Subcutaneous Techniques

These are of scarce interest for problems of equilibrium, but mobilization of the skin
and subcutaneous techniques are useful for diagnosis and treatment of allodynia
areas which are generally residues from vertebral treatment and can perpetuate con-
tinual pain, sometimes deep and widespread, to the patient.
Other interesting techniques are Dicke’s connectival reflexogenic massage,
Teirich-Leube massage, Vodder’s lymphodrainage and Cyriax’s deep massage.
We believe that it is indispensible to know how to use these techniques as they
can lead to a good practice of manipulation and in some cases in its substitution.
27.3.2 Vertebral Manipulation
Vertebral manipulation consists of forced passive mobilization which stretches the

joint elements beyond their physiologic or pathologic barrier up to the limit of
their passive movement. It is called “high speed” or “with impulse”. An abrupt
movement is used in vertebral movement and causes a high-frequency ascending
flux, a rapid proprioceptive re-information to the medulla centres which control
the movement of the articulation. This discharge is therefore able to restore the
normal fluxes to the centres which had become unaccustomed through movement
limitations caused by pain spasms, in our case, after sprain trauma, or owing to
balance or postural problems, even if pain free or caused by previous traumas or
micro-traumas, or for other causes. Some rules must be followed to obtain these
results, such as R. Maigne’s “rule of no pain and reverse movement”, needing the
manipulation to be carried out in the opposite direction to the painful one. The no
pain rule must also be respected in manipulative therapy of equilibrium
problems.
As has been demonstrated through studies on cadavers using accelerometers and

intra-discal pressure gauges [12], the movement of articular heads is slight but
extremely rapid, almost explosive.
Manipulation is not only an antalgic treatment but is above all the first and most
precise and delicate phase of a rehabilitative treatment.
One of the most interesting aspects of this treatment is the possibility to rapidly
modify rachis movement patterns through precise manoeuvres and therefore restore
its function as receptor and effector of equilibrium.
It is indeed in an alteration of the rachis motorial patterns, not only at the cervi-
cal level but also in the thorax and lumbar zones and in their clinical expression,
i.e. DDIM, that we should look for the causes of some equilibrium disorders and
chronic post-whiplash pain, above all at the “passage” level, that is, the passage
zones between one sector and another of the rachis, also called “transitional
zones”.
These zones are:
1. The occipit(o)-atlanto-epistrophei passage
2. The cervical-thoracic passage
3. The thoracic-lumbar passage
4. The lumbar-sacral passage
5. The sacral-coccygeus passage which can also be situated between the 1st and the
2nd coccygeus
Teyssandier describes another functional passage in the medio-thoracic segment
at level T7–T8 [13].
From a clinical point of view, it is advisable to intervene on these passage areas
in order to modify the rachis motorial patterns. R. Maigne has described a “transi-
tional zone syndrome” [14], meaning intervertebral malfunction disorders which
can be situated in two or more passages contemporaneously and all on the same
side.
Vertebral manipulation is not only performed on the proprioceptive afferents but
almost certainly on the vegetative nervous system channels.
Vertebral manipulation may engender vegetative phenomena, such as sweating,
and eliminate other phenomena: closed nostrils and unilateral lacrimation in certain
cervical cephaleas, cutaneous areas of allodynia which instantly disappear, and
therefore they must be related to the vasomotor phenomenons.
In cervical whiplash we find a reduced efficiency both in the dynamic control of
head stability and in the strategies of pelvic control of equilibrium, especially in
brusque disturbances in walking [15].
It is in fact “hip” strategy (hip strategy by Nashner) which controls a vast range
of reactions to destabilizing factors and which appears insufficient in many of the
above-mentioned clinical cases.
By “hips” we refer to: the T-L passage, the L-S passage, sacroiliac and pelvis,
focusing not only on the joints, but also on the motorial coordination obtained
through exact muscular sequences.
This complex sector is also the one which oversees walking, in which, accord-
ing to a recent theory [16], does not originate in the limbs but in the
thoracic-lumbar passage and in the lumbar rachis and is transmitted from here
through the sacroiliacs to the lower limbs which provide the kinetic energy
necessary.
This movement propagates from the lower area up to the first cervical vertebrae
through the anatomic conformation of the cervical joint facets and by the contrast-
ing movement of the humeral-omeric scapular.
The functional synchronization of the phasic muscles of the inferior limbs
and the tonic ones of the spine takes place in the lower passages and moves
upwards [17].
One must never forget that in the damaging mechanism of “whiplash injury”, the
first impact is in the inferior dorsal and lumbar region which is nearly always
involved in this syndrome.
Therefore, we believe that it is necessary to begin treatment on the inferior
passages especially from the lumbar-sacral and then gradually proceed upwards.
The cervical rachis can only be treated after treatments of the inferior levels have
not been able to restore the correct vertebral function.
There are a series of reasons why particular precaution must be taken during
manipulative treatment of the cervical rachis:
A great part of the errors which occur during vertebral manipulation concerns
this zone: such errors are rare but generally serious.
– The major danger has to do with the anatomical situation of the vertebral arteries
and possibilities of undiagnosed past pathologies.
– The importance of the neck in the sphere of the Equilibrium System is because
of the connection of the cervical roots with the vestibular nuclei and also for the
compensation phenomenons which can occur at this level.
– Effective risk-free cervical manipulation calls for great manual and clinical
experience, acquired by the operator, through long formative and practical
training.
In cases of “whiplash” treatment, it is necessary to begin manipulation from
lower vertebral levels, rising gradually, and then treating the neck only if the lesion
is contained in the first two stages of the Quebec Task Force classification WAD
[18], i.e. cervical pain and stiffness without clinical evidence or only with skeletal-
muscle evidence. Even in these cases great caution must be used and manipulation
should not be carried out before 1–3 months have passed, and in full respect of the
treatment rules, always starting with the above-mentioned manual manipulation,
and after having carried out the pre-manipulative tests.
Manipulation techniques should be used to resolve PMID treating the active
ones (spontaneously painful) and the inactive (non-spontaneously painful) when
localized in specific zones: the most significant inactive PMID in this context is
usually located in the “passage area” also called “transition zones” which we have
already mentioned.
It is therefore advisable to begin treatment searching for the PMID, even the
inactive ones, at the lumbar-sacral and mid-lumbar passage, at L3–L4, thus pro-
ceeding with their treatment through mobilization techniques until the correct ten-
sion is reached or with vertebral manipulation with impulse.
Subsequently you seek the PMID, also the inactive ones of the thoracic-lumbar
segment, and then mid-thoracic (D7–D8), and these are preferably treated by the
operator creating an epigastric support extension position.
Then the cervical-thorax segment is treated, also in the absence of PMID, in
extension by the operator using a sternum support position, or with the patient in a
supine position, and always respecting the treatment limits of the specific patient.
In the case of radicular pain pathologies in any of the spinal segments, one must
keep to a “legeartis” treatment, taking all the necessary precautions.
As we have already said, the real cervical treatment must be particularly delicate
and we reaffirm that at this level it is absolutely necessary to correlate the vestibular,
neurologic and algologic physical diagnosis to the vertebral one.
The “compensatory PMID” should never be treated with impulsive manipulation
but only through gentle, superficial stretching. On the contrary, the pathogenic
PMID should be resolved with the use of all Manual Medicine techniques, therefore
starting with post-isometric release and then proceeding with passive mobilization
or “joint play” manoeuvres and if possible concluding with real “high speed” verte-
bral manipulation.
The atlantooccipital segment is where it is more difficult to distinguish between
compensatory “PMID” and pathogenic ones. It is in fact possible, at this level, to
have secondary problems to those of occlusion, or either of ocular fusion or of mono
lateral auditory ones. It is also a zone with high intrinsic risks of both slight and
severe complications. It is therefore advisable to avoid abrupt manipulation and
utilize “gentler” techniques, mainly progressive ones such as fibromyolysis to be
carried out manually with the patient in a supine or sitting position, or simply
through occipit-atlo-epistropheus techniques [19].
One to six sittings twice a week are generally necessary and it is advisable to
carry out a single manipulative movement at the beginning and then to evaluate the
results and add further manoeuvres at higher levels.
In synthesis, the cervical segment can be treated through abrupt manipulation
only in the following cases:
– In the absence of contraindications, especially vascular ones, or of vertebral
instability
– In the presence of active PMID
– In 1st and 2nd grade “Whiplash – associated disorders” (WAD) (TAEC)
– In post-acute phases, rarely in subacute ones and never in an initial acute phase
– Respecting the “no pain rule”
– If treatment of the lower levels has resulted ineffective
– By an expert operator
Conclusion
The elements necessary to proceed to manipulative therapy of after effects of
whiplash (cervical trauma), both for pain or equilibrium dysfunctions, are:
1. Exact neurologic, algologic and equilibrium diagnoses
2. General medical diagnosis, orthopaedic-physiatric and Manual Medicine
diagnosis
3. Competence, ability and experience in Manual Medicine

This procedure could undergo further development through deeper knowl-
edge of the Equilibrium System and of the neuro-motorial control of the rachis.
There are numerous lesions which can pass unobserved in post-traumatic cer-
vical trauma pathology [19]: therefore, manipulation must be carried out with
extreme caution.
Clinical and “treatment” diagnosis of Manual Medicine is the key to manage
a multi-method therapy in which manipulation has a precise indication.
The Quebec Task Force on WI recommends a special preparation for opera-
tors in this difficult field: Manual Medicine, because of its topographic ability in
pain diagnosis, and for the direct treatment which can restore the normal
neuro-motorial control of the rachis, is the appropriate discipline suitable to
teach operators a complete approach to “whiplash” trauma [20–22].
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Rehabilitation Strategy According
to the Quebec Classification 28
S. Negrini, P. Sibilla, S. Atanasio, and G. Brugnoni
28.1 Introduction
Whiplash injuries entail lesions in the cervical spine. There may be elongations
of ligaments, smaller or more serious vertebrae fractures, disc compressions,
prolapses or dislocations of the vertebrae.
The treatment strategy depends upon the type and degree of cervical lesion.
Stabilizing surgery may be indicated in severe cases. Psychological approaches are
a necessity. Simultaneous damage to the brain, brainstem, inner ear, back, pelvis or
lower extremities has to be taken into consideration when planning treatment.
Physiotherapy in whiplash injuries has a central role.
In order to assess the lesions, case history, clinical investigation and imaging
with radiology and MRI are mandatory. This should be performed before the patient
is seen by the physiotherapist.
The manual examination sometimes has to be postponed due to the cervical pain.
The degree of active movement is of importance to notice. Pain may contraindicate
some parts of the examination and physiotherapy, especially in the acute stage.
S. Negrini (*)
Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11,
25123, Brescia, Italy
e-mail: stefano.negrini@med.unibs.it
P. Sibilla
Scoliosis Center, IRCCS “Don Carlo Gnocchi” Foundation, via capecelatro 66, Milan, Italy
S. Atanasio
Istituto Italiano Colonna – ISICO, via Crivelli 5, Milan, Italy
e-mail: salvatore.atanasio@isico.it
G. Brugnoni

292 S. Negrini et al.
Neck hyperextension and dislocation should be noticed and may contraindicate

most physiotherapeutic manoeuvres. One must proceed with caution in implement-
ing neck therapy if the assessment is not performed in an adequate way by the
responsible physician and in some parts completed by the physiotherapist. Cervical
lesions may be worsened by too brisk examinations.
The Bone and Joint Task Force on Neck Pain and Its Associated Disorders [1]
conducted a critical review of the literature on assessment tools and screening pro-
tocols for traumatic and non-traumatic neck pain. According to the Task Force, in
the absence of serious pathology, clinical physical examinations are more predictive
at excluding than confirming structural lesions causing neurologic compression,
that to say the physiotherapist could be, at the same time, the more appropriate
health professional to diagnose and treat a WAD patient.
As usual in the rehabilitation field, attention has been recently more and more
drawn to the biopsychosocial aspects and to the changes in the quality of the lives
of patients who have suffered neck trauma. The strategies of behavioural medicine
intervention are particularly useful, meaning an individual approach with the thera-
pist, with a group or through telematics monitoring. The patient follows a standard
exercise programme at home and therefore should be able to monitor himself and
recognize the changes in his health during daily activities.
To describe the most determinant clinical symptoms, the Quebec Task Force
(QTF) developed in 1995 [2] a classification system which allows a good assess-
ment of the severity of the injury. In cases of QTF I and II whiplash injuries, the
posttraumatic treatment is a domain of conservative therapy. Therapeutic measures
have been exhaustively studied and compared. Physical therapy has been assessed
predominantly with respect to its effects on pain intensity and improving patients’
range of motion. It seems that its efficacy is limited to a certain degree of improve-
ment of these parameters in the acute stage of convalescence. We would like to
emphasize the importance of a multidisciplinary approach within which the psycho-
logical and behavioural aspects are of considerable significance to the rehabilitation
of the patient with WAD (whiplash-associated disorders). Furthermore, we suggest
the distribution of informative pamphlets and the training of the patient by experts
in the emergency departments during the early stages of the post-trauma period.
Early recognition of the patients’ emotional state could be a useful instrument in
shortening the necessary recovery time, reduce eventual unsatisfactory results and
lower the total costs of treatment.
For handling patients with whiplash injuries, a team of specialists is necessary.
The members of different professions need special expertise concerning orthopae-
dics, neurology, neck physiology and neuro-otology. The legal questions can best be
answered by a physician in the whiplash team. The physiotherapist must have a
profound knowledge of neck physiology and treatment, balance problems and ver-
tigo. Education and information of physicians and physiotherapists are necessary to
increase the awareness of the whiplash phenomenon, thereby preventing harmful
delay in treatment and referral.
28 Rehabilitation Strategy According to the Quebec Classification 293
Table 28.1 Clinical Grade Clinical presentation

classification on whiplash-
0 No complaint about neck pain
associated disorders proposed
No physical signs
by the Quebec Task Force
(1995) I Neck complaint of pain, stiffness or tenderness
No physical signs
II Neck complaint
Musculoskeletal signs including:
Decreased range of movement
Point tenderness
III Neck complaint
Musculoskeletal signs
Neurological signs including:
Decreased or absent deep tendon reflexes
Muscle weakness
Sensory deficits
IV Neck complaint and fracture or dislocation
Table 28.2 Clinical spectrum of whiplash-associated disorders as proposed by the Quebec Task
Force (1995) [2]
Grade Presumed pathology Clinical presentation
I Microscopic or multimicroscopic lesion Usually presents to a doctor more than
Lesion is not serious enough to cause 24 h after trauma
muscle spasm
II Neck sprain and bleeding around soft Usually presents to a doctor in the first
tissue (articular capsules, ligaments, 24 h after trauma
tendons and muscles)
Muscle spasm secondary to soft tissue Nonspecific radiation to the head, face,
injury occipital region, shoulder and arm form
soft tissues injuries
Neck pain with limited range of motion
due to muscle spasm
III Injuries to neurologic system by Presents to a doctor usually within hours
mechanical injury or by irritation after the trauma
secondary to bleeding or inflammation Limited range of motion combined with
neurologic symptoms and signs
28.2 WAD Classification
In the literature there has been a great heterogeneity of classifications. The Quebec
Task Force on Whiplash-Associated Disorders proposal represents a milestone for
both clinicians and researchers.
This classification is summarized in Table 28.1. To better compare this classifica-
tion with the one we have proposed, we present, in Table 28.2, other clinical and
pathological specifications proposed by the Quebec Task Force on Whiplash-
Associated Disorders and, in Table 28.3, a summary of our classification.
Table 28.3 Summary of our classification

Degree Lesion Treatment
1st Simple strain Soft collar, 20 days
2nd Strain Soft collar with a good containment, 20 days
3rd Serious strain Hard collar, 25/30 days
4th Compromising of mechanical stability Minerva in Articast, 30/40 days
5th Articular dislocation and/or bony Surgery
fractures
It must be said that we proposed our classification during the S. Margherita

Meeting in January 28, 1995, before the appearance in the literature of the Quebec
Task Force classification. The two are surprisingly similar, but ours is more perti-
nent to our way of treatment and is derived from a more practical, clinical point of
view. The Quebec Task Force classification is designed to better compare the litera-
ture results about different types of patients.
28.3 Whiplash Rehab According to Quebec

Task Force Classification
In this chapter we will discuss the rehabilitative treatment of whiplash, identifying

five clinical degrees of pathology and proposing specific rehab therapeutic
approaches based on clinical evaluation of patient. The rehabilitative tool is particu-
larly focused on the restoration of neck functioning [3–7].
28.4 First-Degree Whiplash
28.4.1 Anatomical Pathology
First-degree whiplash is a simple strain of the cervical spine ligaments. The zyg-
apophyseal joints do not show severe lesions although they have been stressed in
distraction and compression according to the mechanism of injury. In the outer part of
the discs, tears can appear that can justify tardy painful syndromes due to disc protru-
sions. The muscles are stretched, usually without lesions of their bodies and/or their
tendons. An involvement of the sympathetic plexus or nerve roots is seldom [8, 9].
28.4.2 History
The pain is not very accentuated, and is usually local, but sometimes there are irra-
diations to the head and/or shoulders. If trigger points appear, there can be irradia-
tion to the upper extremities, but these are not due to nerve root involvement.
Symptoms usually are increased by active movements and by prolonged periods of
standing and/or sitting. Sympathetic symptoms are rare, but sometimes difficult to treat.
28.4.3 Clinical Examination
If there has been a lateral impact and/or the head of the patient was rotated when the
accident occurred, there can be a torticollis, usually with the head away from the
pain.
28.4.4 Range of Movement
Usually the cervical spine is relatively mobile. Movements are painful in any direc-
tion at the last degrees of the range of movement, and the most involved are exten-
sion and particularly retraction; many times flexion is free. If there is a lateral
component, rotation and lateral flexion are more painful on one side than the other.
It’s important here to remember that rotation tests better assess the upper cervical
spine (occiput-C2), while lateral flexion assesses the medial and inferior
segments.
Testing each articular level it is usually possible to find some joints that are more
involved. This evaluation is fully compatible with the mechanism of the injury:
upper spine if protrusion was prevalent, C5-C6 if flexion-extension was more
important, symmetry if only sagittal movements occurred and asymmetry some-
times with differences between the lower and upper cervical spine if a lateral com-
ponent was present.
It is possible to verify RoM also in the supine position, where there are not many
differences apart from a trivial increase in the RoM.
28.4.5 Palpation
Muscles are not very painful. A light contracture is present, sometimes only in a few
fibres; occasionally trigger points are detectable. Examining the zygapophyseal
joints, it is possible to “feel” their involvement as shown by the RoM segmental
evaluation. Also the lateral apophysis can be painful [5].
28.4.6 Neurologic Examination
It is usually normal.
28.4.7 Diagnosis
There is not real boundary between first- and second-degree whiplash: they describe
a continuum in which the first degree represents the less important clinical lesion
and the second degree represents an important clinical picture, with little move-
ment, significant contracture and frequent irradiation of pain.
28.4.8 Treatment
A soft collar must be prescribed for 10/20 days, because it is necessary to let the
ligaments heal. This happens in 18 days normally [10, 11]. The soft collar permits
a little protected motion inside. It is not possible to move the cervical spine more
than at the beginning of the RoM, but this motion is not only allowable, it is also
advisable. In fact it is known that the ligaments heal along the force lines of the
movement, if this is permitted, if it is not, the ligamentous tissue repairs in a per-
turbed fashion.
Rehabilitation can begin after the collar is no longer needed [12, 13].
28.5 Second Degree
Second-degree whiplash is a real strain of the ligaments and capsules of the zyg-
apophyseal joints. These do not show dislocations: the capsular involvement
depends on their distraction, sometimes internal derangement can be demon-
strated. Disc lesions can be protrusions or bulging. The muscles are over-
stretched, sometimes without lesions of the body: these are more likely to involve
tendons at their insertions. There is usually an involvement of the sympathetic
plexus. The medulla can be slightly stretched, and sometimes nerve roots are
involved too.
28.5.2 History
Pain is local with irradiations to head and/or shoulders. Irradiation to upper extremi-
ties is common, rarely due to nerve root lesions. Active movements are sometimes
impossible, in most cases they are possible only to a minor degree. Vertigo, dizzi-
ness, nausea, vomiting, scotoma and photophobia are common. Sometimes drop
attacks can appear too.
Usually patients present with a fixed position, fully compatible with the mechanism
of injury, including both impact and head position.
The cervical spine is relatively blocked. Movements ar0e painful in any direction at
the very beginning of the RoM: many times the flexion is less involved and the most
involved are rotations. The more blocked movements permit one to understand how
the accident happened.
To test the more blocked articular levels is usually not useful nor possible,
because all of the cervical spine is involved. The RoM in the supine position is usu-
ally a little bit less obstructed.
28.5.5 Palpation
Muscles are painful, usually more at their insertions. An important muscular

contracture is present, usually in trapezium, sternocleidomastoid and elevator scap-
ulae. Trigger points in the same muscles are usually detectable.
Examining the zygapophyseal joints, it is possible to “feel” their involvement
which, at this stage, is normally very important and bilateral, depending on the
mechanics of injury. The lateral apophyses are usually painful.
There can be weakness, sensory impairment and/or reflex alterations. These have to
be monolateral and monoradicular; otherwise it is necessary to evaluate more thor-
oughly the lower extremities and the other neurologic functions to investigate a
possible medullar or central involvement (rare in second-degree whiplash).
28.5.7 Imaging
Reduction of cervical lordosis, localized inversion of the curve or rigidity of a few

segments is more likely in this case.
28.5.8 Diagnosis
As was described above, between second- and third-degree whiplash, the differ-
ences are only clinical: in third degree usually movements are completely blocked
due to the pain, which is more intense and irradiated compared to a second-degree
lesion. Also sympathetic symptoms are more pronounced.
28.5.9 Treatment
A soft collar with good containment (this means that it allows less movement), or a
hard collar must be prescribed for 20 days. It is necessary to pay particular attention
to sustaining the cervical spine without distracting/elongating it. It is also very
important not to keep the cervical spine in an incorrect position: usually patients
with these collars are followed by a technician and not by a physician and this is a
mistake. It is important not to hold the patient in protrusion, because this can be
exactly the position in which the lesion occurred, but to restrain movements keeping
a correct position. If the head is maintained in a protracted position, as long as the
patient is sustained he feels well, but when the collar is removed his symptoms
return, often worsened exactly by the collar. Rehabilitation must begin after remov-
ing the collar. The process must be gradual and determined by the physiotherapist
(according to the physician’s prescription) on the basis of the gradual training of
muscles [14–17].
28.6 Third Degree
Third-degree whiplash is a serious strain of the ligaments that are partially split.
Zygapophyseal joints in this case too do not show dislocations: there is only capsu-
lar distraction and sometimes internal derangements can be demonstrated. Disc
lesions can reach real herniation. Muscles are overstretched, sometimes without
lesions of the body but always of tendons at their insertions. There is an important
involvement of sympathetic plexus. The medulla can be stretched, and nerve roots
usually are involved too [18].
28.6.2 History
Pain is always irradiated to the head and/or shoulders and many times to the upper
extremities due to nerve root lesions. Active movements are impossible and when
the patient is asked to move the neck, he only moves his eyes. Vertigo, dizziness,
nausea, vomiting, scotomata, photophobia and drop attacks are present in most
patients. Sometimes there is tachycardia, pins and needles to both upper and lower
extremities (one or both sides), strength or sensory deficits, eye alterations and
sweating to one upper extremity, revealing significant lesions to nervous
structures.
The patient presents in a fixed position that in this case too is normally a clue to the
mechanism of the injury.
The cervical spine is completely blocked. Active and passive movements are impos-
sible in any direction, although sometimes a little bit of motion appears offering a
clue as to how the accident happened. It is important to be very cautious when

testing RoM in the supine position in these patients.
28.6.5 Palpation
Muscles are painful and very contracted, but palpation at this stage is not very
useful, due to the obvious clinical picture [19, 20].
This exam is very important at this stage, and central signs must be very thoroughly
examined, because as reported in the literature there may also be encephalic involve-
ments. Nerve root signs are not rare.
28.6.7 Diagnosis
Between third- and fourth-degree whiplash there is a definite boundary: a radio-

graphically evident lesion with sub-dislocation of zygapophyseal joints.
28.6.8 Treatment
A hard collar must be prescribed for 25–30 days. In these cases it is important to offer
a support to both chin and occiput. Many times it is also necessary to extend anteri-
orly to the sternum, blocking in this way the possibility of moving the head anteriorly
or maintaining an incorrect position. Obviously not distracting/elongating the cervi-
cal spine nor keeping an incorrect position is crucial here. Rehabilitation must begin
after removing the collar and must be very gradual. The collar must be removed
gradually over 15–30 days, always determined by the physiotherapist according to
the physician’s prescription and closely monitoring training of the muscles [21–24].
28.7 Fourth Degree
Fourth-degree whiplash is a condition in which the mechanical stability of the cervical

spine has been compromised. There is a capsular disruption of zygapophyseal joints
combined with a ligamentous strain that allows pathological movements between ver-
tebral bodies. In this case too disc lesions such as definite herniation are common.
Neurological lesions can include all of what has been described above together with a
possible direct compression of nerve structures. A medullar damage can be suspected,
but sometimes it appears only later rather than immediately after the injury occurred.
28.7.2 History
Pain is particularly important and does not respond to treatments. Active move-
ments are impossible. All neurological symptoms mentioned above can be pre-
sented by the patient.
There are not important differences from what has been mentioned regarding third-
degree whiplash.
28.7.4 Diagnosis
Between fourth- and fifth-degree whiplash, there is another definite boundary: a

complete articular dislocation [25–27].
28.7.5 Treatment
A Minerva collar in Articast (less heavy than one in simple cast) has to be pre-
scribed for as long as 30–40 days, assuring in this way a complete blockage for a
period long enough to permit stabilization. If this does not occur, it is necessary to
stabilize the cervical spine surgically. The rehabilitation process must be as pre-
sented above [28–31].
28.8 Fifth Degree
This lesion is not completely pertinent to our work. It is very rare, it has a dramatic
clinical picture and it is characterized by dislocation of one or more articular pro-
cesses or by bony fractures.
The risks are very high and it is necessary to act surgically to reduce the lesion
with an anterior or posterior fusion.
28.9 To Immobilize or Not to Immobilize:

That Is the Question
We discuss this issue because our proposal is somewhat different from what can be
found in the recent literature. One of the biggest problems that we have to face
nowadays regarding harmless spinal pathologies is if rest or early mobilization is
the best treatment. In some ways, low back pain and whiplash injury are similar
because the general consensus of treatment by rest (should it be bed rest or collars)
has shifted to a less general, but still common, consensus in promoting mobility as
early as possible.
The Quebec Task Force on Whiplash-Associated Disorders stated: “Based on
limited evidence and reasoning by analogy, it is the Task Force consensus that the
use of non steroid anti-inflammatory and analgesics, short-term manipulation and
mobilization by trained persons, and active exercises are useful in Grade II and III
WAD, but prolonged use of soft collars, rest or inactivity probably prolongs disabil-
ity in WAD”.
In any case, this consensus does not mean that it is proven that mobilizing is the
correct answer to the problem, particularly in the case of a whiplash-injured patient.
We have to remember that:
• All the studies addressing the problem have evaluated short-term disability, but
we know that long-term results should be the most important for this type of
patients.
• Soft collars do not immobilize the neck, but only restrict wide-range
movements.
• Mobilization must be in any case a step in the treatment that we proposed, but
this does not mean that must it be the first one.
• Many times the inadequate results of patients that have used a collar are due to
the lack of a good rehabilitative process after removing the collar.
• Doctors must not abdicate their role of making the diagnosis and choosing treat-
ments according to the level of pathology: research results say only what is better
for most (statistical significance), not for all.
Bearing in mind these points, we think that it is not sound to propose, as many
do, that mobilization should be prescribed until it has been shown that immobiliza-
tion is superior to mobilizing interventions.
Whiplash is presumably a form of distortion of the cervical spine. This patho-
genic mechanism acts on a composed structure made up of many articulations, a
large quantity of muscles with a very fine regulation and large bands with a stabiliz-
ing, not a blocking, function.
A general rule is that ligamentous or capsular stretchings require immobilization
as a means of repair. This must be prolonged to at least 18 days to be effective.
Immobilization can be partial or total according to the severity of pathology; it is
also possible to prolong the immobilization time according to necessity.
The real goal of treatment is to avoid over time pain and development of a
possible instability at a distance. Our experience over the years has taught us that
a cervical, whiplash-injured spine that did not remain immobilized sufficiently
can more frequently cause problems and that these problems last for a longer
time.
Therefore, mobilization is possible only if the trauma is so minor that there has
not been a real lesion of ligamentous structures, but only a lengthening. If there is
an involvement of capsules, ligaments or tendons, it will be necessary to immobilize
[32–36].
We think that only when mobilization proves more effective than immobilization
will it be possible not to observe these cautious rules.
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Whiplash-Associated Equilibrium
Disturbances (WAED) Rehabilitation: 29
Vestibular Re-education
and Vestibular Rehabilitation
D.C. Alpini, A. Cesarani, and F. Di Berardino
29.1 Introduction
The human equilibrium system derives much of its strength and plasticity from the
fact that the specific neuronal and growing software is moulded in childhood during
the maturation phase, under the influence of permanent information from the world
we live in. The software overlying the structural, sensorial and central nervous hard-
ware creates the so-called space concept within the brain. Post-whiplash failures of
the sensory inputs as well as of the central equilibrium regulation may lead to ver-
tigo, blurred vision, static and/or dynamic head and body instability. The system has
many inborn possibilities for internal stabilization and compensation; in fact after
injuries there are different neurophysiological phenomena involved in the restora-
tion of the equilibrium function [1, 2].
Rehabilitation specifically acts activating one or more of these phenomena [3].
They are:
Restitution can be defined as a complete reparation after a temporarily limited
lesion.
Adaptation means that the human equilibrium system can adapt itself to physiologi-
cally, as well as to pathologically, altered conditions. The central regulatory sys-
tem can reweigh sensitivity of the vestibular, retinal and other receptors used to
D.C. Alpini (*)

ENT-Otoneurology Service, IRCCS “Don Carlo C. Gnocchi” Foundation,
Milan, Italy
A. Cesarani • F. Di Berardino
Milan, Italy
Milan, Italy
e-mail: antonio.cesarani@unimi.it; federica.diberardino@unimi.it

regulate equilibrium. It comprises all phenomena which ensure that a patient

with a persisting peripheral dysfunctional state reattains a normal – or near
normal – behaviour in relation to his space orientation and balance in rest as well
as when executing movements. He again maintains his erect standing position
and has no more “odd” feeling categorized as vertigo or dizziness. The messages
sent by the sense organs into the brainstem are more and more suppressed and
prevented from reaching the higher centres the longer the steady state in the sur-
rounding world persists. The subject has adapted itself to conditions imposed by
the outer world. Yet the slightest change in stimulatory conditions not pertaining
to the steady state will alarm.
Habituation is defined by the reduction of the intensity and duration of the subjec-
tive vestibular reactions, for example, vertigo and nausea in the case of seasick-
ness. Habituation is a term used in the sense that repeated exposure to a
“mismatched” sensory situation (e.g. during caloric testing, postural vertigo,
motion sickness conditions) induces such changes in the central processing as to
annihilate the undesirable effects and to do so with a prolonged effect. It has been
based upon the development of conditioned compensatory reactions to oppose
inappropriate responses associated with visuo-vestibular conflicts and exposure
to unusual motion environments.
Compensation describes another type of central nervous counter-regulation as a
result of functional deterioration due to a vestibular or other equilibrium lesion.
It utilizes supplementary functions which are added so that an overlay of addi-
tionally activated functions covers the underlying equilibrium lesions by mean
of its neuronal plasticity. However, primary lesion continues to exist and can, in
the case of a special conflict, manifest itself in the clinical phenomenology. It is
a goal-directed process induced by some recognized “error” in the system and
directed to its elimination. Thus compensation may be defined as an error-
controlled goal-directed learning process.
These phenomena lead to different levels of recovery. Recovery is essentially
due to the integration of different level of substitution:
Sensorial substitution, in which the movement of the subject is identical to the one
before the lesion but the subject uses different set of sensory receptors for trig-
gering and control
Functional substitution, in which the neuronal mechanisms subtending the move-
ment have been changed but still belong to the subsystems normally used by the
subject
Behavioural substitution, by which the nervous system calls for new motor behav-
iours not belonging to its normal repertoire
Under another point of view, the evolution of a lesion can be interpreted into
three stages of damage:
– The primary damage: the lesion that induces the onset of symptomatology
– The secondary damage: the pathological modification of the compensatory
systems
– The tertiary damage: chronicization of pathological adaptive phenomena
Treatment had to be pointed to limit primary damage (usually by means of
pharmacotherapy), to reduce secondary damage and to avoid tertiary damage.
29 Whiplash-Associated Equilibrium Disturbances: Rehabilitation 307
29.2 Vertigo
Benign paroxysmal positional vertigo (BPPV) is due to displacement of otoconia as

a consequence of the head concussion during whiplash, and BBPV is the most com-
mon cause of vertigo caused by vestibular pathology; it is very frequent after head
trauma but this is not the case after whiplash. Anyway, it has to be taken into account
also in whiplash-associated equilibrium disturbances (WAED) patients: whiplash-
associated BBPV (WA-BPPV).
The characteristic presentation of this disorder involves repeated episodes of the
transient illusion of spinning, triggered by head motion in the plane of the involved
semicircular canal (SCC). Cupulolithiasis and canalolithiasis [4] have both been
proposed as pathophysiologic mechanisms underlying BPPV. Canalolithiasis,
involving free-floating otolithic particles moving within the affected SCC, is
responsible for the majority of WA-BPPV cases. Of the three SCCs, the posterior
SCC is most commonly affected because of its anatomical location inferior to the
utricle.
Most cases of WA-BPPV can be treated using physical therapy, with the Epley’s
[5] canalith-repositioning procedure (CRP) in the case of canalolithiasis and
Semont’s [6] liberatory manoeuvre in the case of cupulolithiasis, both acting through
restitution phenomenon. In this sense these kinds of procedures have to be consid-
ered in vestibular re-education.
Although both manoeuvres have been shown to have therapeutic benefits, they
require sequential procedures involving moving the patient’s head and body into
unnatural positions, making them sometime unsuitable for WAED patients with cer-
vical or back disorders, especially for older patients.
In WAED patients, it is thus better to use more conservative procedures like the
supine to prolonged lateral position (SPLP) [7] or the rolling-over manoeuvre
(ROM) [8].
SPLP contained two steps. First, the patient was instructed to start in an upright
sitting position and then lie down supinely on the bed and maintain this position for
3 min. During this step, it was proposed that the trapped otolithic particles would
move away from the ampulla (ampullofugal), drift towards the common crus by
crossing the horizontal SCC plane and stay in the superior arm of the posterior SCC.
In the second step, the patient was asked to sleep on their healthy side by turning
their head and body from the previous supine position towards the healthy side lat-
erally. This process allowed the particles to slip through the common crus into the
utricle. To facilitate their movement back into the utricle and to prevent any floating
particles in the utricle from being trapped in the posterior SCC again, a prolonged
side lateral position (minimum duration 30 min) was suggested at bedtime, with or
without a pillow support.
ROM involves moving the patient from supine to nose-up position to a right ear-
down position and maintaining this position for 10 s, before subsequently returning
the head to a nose-up position, which is maintained for further 10 s. The patient is
then moved to the left ear-down head position which is maintained for 10 s. Patient
repeats these manoeuvres 10 times in a set and two sets in day, before getting up in
the morning and before sleeping in the night.
ROM can be performed either by neck rotation or by whole-body movements

without any cervical torsion. This is very suitable for whiplash patients, especially
in the early phases of trauma.
29.3 Dizziness and Disequilibrium
Dizziness and disequilibrium following whiplash may be recovered by means of

vestibular rehabilitation, which is a special rehabilitation of motion intolerance and
imbalance problems. Although it has only recently gained wide attention, the con-
cept of head, body and coordinated eye exercises as a treatment for vestibular disor-
ders is actually over 50 years. As far back as the mid-1940s, an English otolaryngologist
Sir Cawthorne [9] observed that some patients who experienced dizziness did better
or recovered sooner when performing rapid head movements. In cooperation with a
physiotherapist, Cooksey, he developed a regimen of exercises which, with some
modifications, are frequently still used today. Cawthorne-Cooksey [10] protocol is
based on the concepts of habituation and sensory substitution (Table 29.1).
Vertigo and dizziness are conscious symptoms and the disturbances are not dis-
equilibrium or nystagmus but the consciousness of disequilibrium and nystagmus.
Thus physical rehabilitation must not only be pointed to resolution of objective
disorder but it must be aimed to resolution of subjective consciousness of the disor-
der itself. Such a particular kind of treatment needs a particular theoretical basis.
This is the reason why we structured our method of rehabilitation on a particular
model of the vestibular system: the MCS method [11–13]. MCS is the acronym of
mechanic, cybernetics and synergetics [14].
Table 29.1 Cawthorne-Cooksey Protocol
Exercises
In Bed
1. Eye movements, at first slow, then more quickly: (a) Up and down. (b) From side to side.
(c) Focusing on fingers moving from 3 feet to 1 foot away from head.
2. Head movements, at first slow, then quick. Later with eyes closed. (a) Bending forwards
and backwards. (b) Turning from side to side.
Sitting
1. Eye movements as above.
2. Head movements as above.
3. Shoulder shrugging and circling.
4. Bending forwards and picking up objects from the floor.
Standing
1. A-1 & A-2 & B-3 as above.
2. Changing from sitting to standing position with eyes open and with eyes shut.
3. Throwing a small ball from hand to hand, above eye level.

4. Throwing ball from hand to hand, under knee.
5. Change from sitting to standing and turning around in between.
Dynamic
1. Circle around the centre person who will throw a large ball and to whom it will be
returned.
2. Walk across room with eyes open and then eyes closed.
3. Walk up and down slope with eyes open and then closed.
4. Walk up and down steps with eyes open and then closed.
5. Any games involving stooping and stretching such as frisbee, catch or basketball.
Under a mechanic point of view, we can consider the equilibrium function as the
result of the sum of vestibular reflexes, the contemporary but distinct activation of
some or all of these reflexes, according to the need: gaze, standing and walking.
Under a cybernetics [15] point view, all the structures, peripheral and central, that
contribute to the balance ocular reflexes (BOR) and balance spinal reflexes (BSR)
[16] constitute a system, that to say, a network of different structures interconnected
and interacting to reach a common goal. In this case the goal is human balance.
Under a synergetic point of view, equilibrium is the result of integration different
functional levels, orientation and coordination [17].
On the basis of MCS model of equilibrium system, different protocols for the
different vestibular impairments have been prepared, including WAED patients.
Protocols combine physical and instrumental exercises and they are subdivided into
a part to be executed with the physiotherapist in the gymnasium and in self-
administrated exercise, at home.
From an MCS point of view, WAEDs are caused by distortion and desynchroni-
zation of the proprioceptive chain:
– Modification of the proprioceptive cervical inputs to the vestibular nuclei and
reticular formation
– Desynchronization between vestibular cues and general cervical inputs regarding
head position and movement
– Modification of the cervico-spinal reflexes
– Head-to-trunk dynamic stabilization
Treatment is pointed to:
1. Restore cervico-dorsal mobility
2. Restore dorsolumbar mobility
3. Reorganize proprioceptive informations from the neck and the pelvis
4. Avoid secondary damage characterized by reduction of the movement of the
body along the neck with involvement of the thoracolumbar segment and the
pelvis
5. Restore head-neck coordination
6. Restore the control of head stabilization during gait
7. Reorganize self-perception of posture
Because whiplash injuries cause different and variable damage and symptoms,
the following protocol is only a general guide about what action we think is useful in
patients after such a trauma. In every patient suffering vertigo and balance disorders,
but especially in WAED cases, treatment closely tailored to the patient is necessary.
Rehabilitation may be combined also with pharmacotherapy (see Chap. 19) like
decontracturings or myorelaxants (Diazepam) or L-sulpiride (at low doses). If cog-
nitive functions are compromised, nicergoline or citicoline may be useful. If cervi-
cal proprioceptors are hyperactive, cinnarizine or flunarizine may be used at low
doses for a short period.
Physical exercises are reported in Tables 29.2 and 29.3, while instrument-assisted
treatment is described in the specific following chapters.
Table 29.2 MCS Physical Exercises
I Week: Mechanics Phase

Goals:
• Enforcement of extensor antigravity muscles
• Mobilization of ankle and pelvis joints
Exercises:
The patient takes his two knees to the chest, contemporary, helping and softly, with the hands
With the flexed legs and the feet on the bed, the patient rotates his pelvis rightwards and
leftwards keeping his knees flexed and your legs united
The patient lifts his pelvis taking contemporary his arms extended over his head. Then
he retakes his arms along the body lowering his pelvis
In quadrupedal position the patient extends contemporary the right arm and the left leg.
Then he repeats with the left arm and the right leg
In prone position the patient lifts his left arm and the right leg maintaining his forehead
over the bed. Then he repeats with the right arm and the left leg
The patient repeats as above but lifting contemporary also the head
The patient inhales. Exhaling, he bends forwards taking his head on the right knee. He
waits 10 s. Inhaling he returns in sitting position. Exhaling, he bends forwards taking his
head on the left knee. He waits 10 s and then inhaling he returns seated
II Week: Cybernetics Phase

Goals:
• To improve interaction between ocular and spinal performances
Exercies:
The patient fixates a target on the ceiling and slowly moves his head rightwards and
leftwards
The patient looks for two equidistant targets on the ceiling, and then he fixates them
alternatively first moving only the eyes and then moving only the head
The patient from supine position passes to the sitting position fixating a point straight in
front of him
From the supine position, the patient passes to the sitting position fixating a point sited
on his right
From the supine position, the patient passes to the sitting position fixating a point sited
on his left
The patient goes up and down a step, fixating a target according the following sequence:
Right foot up Left foot up Right foot down

Left foot down Left foot up Right foot up
Left foot down Right foot down
Then he repeats with eyes closed
III Week: Synergetics Phase

Goals:
• Integration of cognitive and motor performances
Exercises:
The patient extends his right arm and lifts his thumb. Then he moves slowly his arm to
and fro before along a horizontal direction and then along a vertical direction. The patients
is instructed to pursue his thumb with eyes only, first slowly and then increasing progres-
sively the velocity of thumb displacement.
After that, he has to perform the exercise as above but moving contemporary also the
head trying to maintain the eyes still.
The patient opens a book in front of him. Then he sends it away from him extending his
arms reading it. Then he brings it near to him slowly, trying to read it. Then he sends it away
again and he repeats some times to and fro.
Table 29.3 Home Protocol
Exercises have been subdivided according to different phases of equilibrium, from supine
to standing to moving. In each phase, there is a progression from mechanic to synergetics
exercises
Home exercises cannot ever substitute the therapeutic programmes showed in the previ-
ous chapter performed with the therapist. Home exercises complete the therapeutic period
and maintain the obtained results.
Supine
1. Take your two knees to the chest, contemporary, helping and softly, with the hands
2. Put a pill under your leg. Bound a 2 kg weight on your ankle with the flexed knee; then
extend it alternating the right and left legs
3. With the flexed legs and the feet on the bed, rotate your pelvis rightwards and left-
wards keeping your knees flexed and your legs united
4. Lift your pelvis taking contemporary your arms extended over your head. Then retake
your arms along the body lowering your pelvis
5. Fixate a target on the ceiling and slowly move your head rightwards and leftwards
6. Look for two equidistant targets on the ceiling and then fixate them alternatively, first
moving only the eyes and then moving only the head
(continued)
7. In the quadrupedal position, inhale and arch your back (hyperkyphosis) taking your
head between your arms. Then exhale bending your head and rotating the pelvis in
hyperlordosis
8. From supine position pass to the sitting position fixating a target straight in front of
you
9. In quadrupedal position extend contemporary the right arm and the left leg. Then
repeat with the left arm and the right leg
10. In prone position lift your left arm and the right leg lifting contemporary also the head.
Then repeat with the right arm and the left leg
Sitting
11. Extend your right arm and lift your thumb. Move slowly your arm to and fro before
along a horizontal direction and then along a vertical direction. Pursue your thumb
with eyes only, first slowly and then increasing progressively the velocity of thumb
displacement
12. As in the previous exercise but moving contemporary also the head trying to maintain
the eyes still
13. Move your head first slowly and then faster in all directions fixating a target straight in
front of you
14. Inhale. Exhaling, bend forwards taking your head on the right knee. Wait 10 s. Inhaling
return in sitting position. Exhaling, bend forwards taking your head on the left knee.
Wait 10 s and then inhale and return seated
15. Inhale. Exhaling bend forwards to keep an object on the floor. Inhale and take it up
over your head and then fixate it for 10 s. Inhale. Exhaling bend forwards and take the
object on the floor
16. Open a book in front of you. Read it moving, contemporary, the book right and left and
then to and fro
Standing
17. Fixate yourself in a mirror. Align correctly your position. Maintain equilibrium for
1 min and then close your eyes looking your correct position in your mind and remain
in this position for at least 1 min
18. Repeat the same, standing on a soft mattress
19. Fixate yourself in a mirror; then, keeping your feet still, bend your trunk to and fro and
right and left with eyes closed standing on a soft mattress
20. Keep a little object and lift it over your head. Fixate it. Inhale. Then exhale and bend
yourself forwards taking the object on the floor. Wait 10 s and then inhaling lift again
the object over your head
21. Standing on soft mattress, keep a little object and lift it over your head. Fixate it. Lift
it over your head and then, with your straight arms, move the object drawing circles
and, bending contemporary your trunk and your knees, after that take it on the floor
Moving
22. Stepping with eyes closed, moving the head to and fro
23. Stepping, reading a book
24. Stepping on a soft mattress, reading a book
25. Go up and down a step, moving to and fro your head, according the following
sequence:
Right foot up Left foot up Right foot down

Left foot down Left foot up Right foot up
Left foot down Right foot down
References
1. Bronstein AM, Brandt T, Woollacott MH (eds) (1996) Clinical disorders of balance, posture
and gait. Arnold, London
2. George FH (1962) The brain as a computer. Pergamon Press, Oxford
3. Claussen CF (1994) Vestibular compensation. Acta Otolaryngol (Stockh) 513(Suppl):33–36
4. Rajguru SM, Ifediba MA, Rabbitt RD (2005) Biomechanics of horizontal canal benign parox-
ysmal positional vertigo. J Vestib Res 15(4):203–214
5. Epley J (1992) The canalith reposition procedure: for the treatment of benign paroxysmal
vertigo. Otolaryngol Head Neck Surg 107:399–404
6. Semont A, Sterkers JM (1980) Reeducation vestibulaires. Les Cahiers D’Orl 15:305
7. Shih CP, Wang CH (2013) Supine to prolonged lateral position: a novel therapeutic maneuver
for posterior canal benign paroxysmal positional vertigo. J Neurol 260(5):1375–1381.
doi:10.1007/s00415-012-6807-9
8. Sugita-Kitajima A, Sato S, Mikami K, Mukaide M, Koizuka I (2010) Does vertigo disappear
only by rolling over? Rehabilitation for benign paroxysmal positional vertigo. Acta Otolaryngol
130(1):84–88
9. Cawthorne T (1944) The physiological basis of head exercises. J Chart Soc Physiother 30:106
10. Dix DR (1974) Treatment of vertigo. Physiotherapy 60:380
11. Cesarani A, Alpini D (1991) New trends in rehabilitation treatment of vertigo and dizziness.
In: Akyildiz N, Portmann M (eds) Vertigo and its treatment. Proceedings of international sym-
posium for Prof. G. Portmann’s Centenary, Ankara, 16–18 May 1990, Ankara, pp 90–104
12. Cesarani A, Alpini D (eds) (1994) Equilibrium disorders. Brainstem and cerebellar pathology.
Springer, Milano
13. Cesarani A, Alpini D (1999) Vertigo and dizziness rehabilitation. Springer, Milan
14. Gluck MA, Rumelhart DE (eds) (1990) Neuroscience and connectionist theory. Lawrence
Erlbaum Associates Publishers, Hillsdale
15. Ashby WR (1956) An introduction to cybernetics. Chapman & Hall, London
16. Norrè ME (1990) Posture in otoneurolog. Acta Otorhinolaryngol Belg 44(2–3):55–364
17. Haken H (2006) Synergetics of brain function. Int J Psychophysiol 60(2):110–124
Vestibular Electrical Stimulation
30
A. Cesarani, D.C. Alpini, and E. Filipponi
30.1 Introduction
Peripheral proprioceptors of the muscles and the joints have a feedback control on
the vestibular nuclei through the spino-vestibular pathways. Neuromuscular spin-
dles and Golgi receptors are dynamometers and they are particularly sensitive to
variations in muscle length and tension. Joint receptors, Ruffini and Golgi bodies,
give information regarding the position of a joint and its movement. The portion of
the neck including the first three vertebrae is particularly involved during the major
part of everyday head movements [1, 2].
The paravertebral muscles of this region are very rich in proprioceptors. They are
especially concentrated in the splenius capitis, the rectus capitis major, the longis-
simus capitis, and the semispinalis capitis. These muscles comprise the deep plane
of the nuchal muscles. The splenius is more superficial. The muscles act in the
extension of homolateral bending and rotation of the head. During head movements
they discharge to the vestibular nuclei [3, 4].
A. Cesarani
D.C. Alpini (*)
E. Filipponi
S.I.T.R.A. (Rehabilitation) - Audiology Unit,
IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico, Milan, Italy

It is known that vibration of muscles or muscle tendons alters proprioceptive

input and produces kinesthetic illusions in human subjects. A lot of clinical and
experimental evidence exist regarding the effects of vibration of the paravertebral
muscles on posture control and head-trunk coordination. Generally the effects are
based on the activation of the cervico-spinal reflexes (CSRs): bending the neck and
turning the head relative to the body evokes reflexes in the limb muscles either in
decerebrate cats [4] or in human beings [5].
It is possible [6–8], in the absence of any actual movement, to induce kinesthetic
illusions and associated motor responses in humans when mechanical vibrations are
applied either to the distal tendon of a limb muscle or to the neck. Illusory move-
ments and/or motor responses can be extended to the whole body when vibrations
are applied to muscles involved in postural stance, such as neck muscles.
Vibration therefore constitutes an efficient means of obtaining true copies of
actual sensory messages and thus eliciting “at will” illusory movements, the direc-
tion, speed, and duration of which can be preselected.
Vibration of the posterior muscles of the neck has been shown to induce illusions
of changed position and of motion of a visual target when the target is presented
with no visual background [9].
Cervical muscle proprioceptors are sensible to superficial electrical stimula-
tion (SES), too. SES is a noninvasive technique that provides nerve and/or muscle
stimulation by means of surface electrodes. The characteristics, the size, and the
site of application of the electrodes and the characteristics of the electrical waves
play a fundamental role in the neurophysiological effects of the SES. Our previ-
ous experimental experiences [10–16] showed that vibration of the paravertebral
muscles can be substituted by SES. Usually, handheld antalgic electrostimulators
are called TENS stimulators, which means transcutaneous electrical nerve stimu-
lations [17]. The excitation of the peripheral motor nerves and the associated
muscle activation is caused by the application of an electric current to the skin,
which usually corresponds to the motor points. This kind of stimulation induces
depolarization of the motor nerves either in the centrifugal or in the centripetal
sense. Furthermore this kind of stimulation induces an activation of the sensitive
nerves of the skin. Thus it is difficult to divide the motor and the sensitive effects
of the SES.
Lackner [7] remarked that the vestibular nuclei are really polysensorial relays
and that they are not only labyrinth correlated. The author underlined that it is not
possible under natural circumstances to activate the vestibular receptors without
implicating other force-sensitive receptor systems that convey information relevant
to spatial orientation.
On the basis of this extensive, but physiologically justified, point of view of the
vestibular system, we refer to superficial paravertebral electrical stimulation as ves-
tibular electrostimulation (VES).
It was shown that neurophysiological effects of VES are strictly dependent on
the characteristics of the electrical wave. Thus the definition of VES pertains only
to those waves able to induce measurable neurophysiological cervico-spinal effects.
30 Vestibular Electrical Stimulation 317
Fig. 30.1 The device
30.2 The Device
Either for experimentations or for clinical application, we used an electrostimulator,

agar. It is a small (25 × 36 × 91 mm) and light (88 g) portable device prepared at
Hadassah University Hospital of Jerusalem (Israel) and approved by the US Food
and Drug Administration.
The mean currency intensity is 0.9 pAlmm2 and the impulse currency intensity is
30 CLA/rnm2, the maximum impulse power is 5 W, the maximum impulse charge
is 22 p C, and the mean impulse charge is 0.55 C.
The device is able to produce different stimulation modes (Fig. 30.1).
Burst. This consists of short pulse series at a high frequency repeated at slow
frequency. This stimulation mode is used for pain relief. The stimulation should be
so strong that muscle contractions can be seen. Usually the electrode is placed on a
large muscle near the aching spot. Burst is not useful for vestibular stimulation.
30.2.1 TENS
It consists of short electric impulses and is used for pain relief.

The stimulation must never be so strong that muscle contractions are found.
The electrodes are normally placed on nerve paths leading away from the aching
spot. Sometimes this wave can be varied as regards both pulse width and stimula-
tion currency. The variations are random but pulse width multiplied by stimulation
current is constant (i.t. = constant charge). This stimulation mode prevents tolerance
to a set pulse width.
Muscle Stimulation Used for Rehabilitation of Muscles. The stimulation should
be so strong that the muscles contract. The stimulation consists of stimulation (on
time) with a slow rise (rise time) and a pause (off time). This sequence is repeated
and makes the muscle slowly contract and be tight for some time. It is often used on
weak muscles (rehabi1itation); the stimulation frequency is kept low (20–30 Hz) to
avoid tiring out the muscle. For sports training higher frequencies are used. This
wave is not useful for vestibular stimulation.
30.2.2 VES
This is an electric stimulation of cervico-dorsal muscles by using a biphasic asymmetri-

cal modulated square wave. The modulation program randomly modifies the duration of
each wave. The mean duration is 100 ps while the frequency is 80 Hz. Electrodes are
small (2 cm2) and placed at a distance of 1 cm from each other. A pair of electrodes
stimulates paravertebral muscles at the level of the second cervical vertebra, and a pair
stimulates the contralateral superior trapezius. The intensity of VES is never able to
induce muscle contractions. The frequency used is in the muscle spindle range of vibra-
tory activation (80 Hz). Thus, it is likely that VES activates the same spinal pathways of
the CSRs. VES modulates the lower limbs postural reflexes in the same way.
Vibratory stimulation of muscle in a range between 1 and 100 Hz is able to acti-
vate muscle spindles. The vibratory stimulation of the neck muscles produces pro-
prioceptive inputs to the brainstem. These afferent volleys are able to evoke postural
reflexes from the muscle of the lower limbs: CSRs. By means of the same mecha-
nism, vibration is also able to evoke alterations of the perceptual representation of
the shape and orientation of the whole body and/or body parts.
The experimental results obtained by VES show that this kind of stimulation
clearly influences the excitability of the motor neurons of the lower limbs. This
influence resembled the action of CSRs on the extensor lower muscles (see Chap.
31 by Osio et al.).
Alteration of proprioceptive input from the neck by VES led to changed percep-
tion of head position. The manipulated proprioceptive input is incorporated in the
head position signal with any other input contributing to head and body position
control [18, 19].
30.3 Indications
After whiplash injuries, two conditions are especially indicated for VES treatment:
1. Paroxysmal positional vertigo
2. Unsteadiness and dizziness with VOR (vestibuloocular reflex) and/or VSR
(vestibulospinal reflex) asymmetry
Posttraumatic positional vertigo is, generally, atypical: it is often bilateral, not
resolved by Semont maneuver. Nystagmus has no latency or it does not decrease by
repeating the movements.
Usually we treat the patient with one or two Semont maneuvers. When they are
uneffective we employ VES. The electrodes are placed on the cervical paravertebral
muscles ipsilateral to the fast phase of positioning nystagmus (that is usually con-
cording with the vertiginous position) and on the contralateral trapezius. Each stim-
ulation lasts 30 min. During stimulation the patient walks or performs simple and
30 Vestibular Electrical Stimulation 319
provocative rehabilitative exercises such as Cawthorne-Cooksey protocol.

According to intensity of the symptoms, the patient is treated once a day for 5 days
a week for 2 weeks or once a day every 2 days for 2 weeks.
When paroxysmal positional vertigo is bilateral, cervical electrodes are placed
on the most intense side if there are no important VOR and/or VSR asymmetries.
When unsteadiness is associated with asymmetrical vestibular reflexes, the cer-
vical electrodes are placed on the opposite side of the VOR hyporeflexia and/or
Romberg deviation and/or stepping deviation. In some cases VOR hyporeflexia is
not accompanied by ipsilateral stepping and/or Romberg deviation. This can be
generally due either to the modification of the postural dynamic caused by the
trauma or to pre-trauma postural conditions.
In these cases it is sometimes difficult to interpret if VOR prevalence compen-
sates VSR deficit or if postural asymmetries compensate VOR hyporeflexia or if
previous musculoskeletal conditions induce unexpected VSRs.
In these cases the sites of stimulation cannot be standardized but have to be cho-
sen on the basis of a complete postural evaluation and a complete neuro-otological
examination with special regard to smooth pursuit, optokinetic nystagmus, and
VVOR (visuo-vestibuloocular reflex).
The general rule is that cervical electrodes are placed on the prevalent site and
the trapezius electrodes are placed on the deficit site.
The treatment protocol lasts 2 weeks (a stimulation once a day) or 3 weeks (a
stimulation every 2 days).
VES is frequently used to prepare the patient for rehabilitative treatment when
vertigo and dizziness provoked by head/body is intense. There is no contraindica-
tion in the combination OWES and some early orthopedic treatment such as the
collar. Obviously, in these cases VES is performed without the collar.
VES is particularly indicated starting “equilibrium rehabilitation”, in the early
phases of the trauma, and to treat also “low compliance” patients.
Some simple tasks during VES improve the effects of the treatment and the best
results have been obtained combining VES and some cognitive involved rehabilita-
tion procedures such as center of gravity visual feedback reeducation.
References
1. Berthoz A, Llinas R (1974) Afferent neck projection to the cat cerebellar cortex. Exp Brain
Res 20:385–401
inputs on vestibulospinal neurons. J Neurophysiol 45:852–866; Biguer B, Donaldson IML,
Hein A, Jannerod M (1988) Neck muscle vibration modifies the representation of visual
motion and direction in man. Brain 11(1):1405–1424
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ence, 3rd edn. Elsevier, New York, pp 596–607
4. Brink EE, Suzuki I, Timerick SJB, Wilson VJ (1985) Tonic neck reflex of the decerebrate cat:
a role for propriospinal neurons. J Neurophysiol 54:978–987
5. Dumas G, Lion A, Gauchard GC, Herpin G, Magnusson M, Perrin PP (2013) Clinical interest
of postural and vestibulo-ocular reflex changes induced by cervical muscles and skull vibration
in compensated unilateral vestibular lesion patients. J Vestib Res 23(1):41–49
6. Kobayashi Y, Yagi T, Kamio T (1988) The role of cervical inputs in compensation for unilat-
eral labyrinthectomized patients. Adv Otorhinolaryngol 42:185–189
7. Lackner JR (1988) Some proprioceptive influences on the perceptual representation of body
shape and orientation. Brain 111:281–297
8. Lackner JR (1992) Multimodal and motor influences on orientation: implications for adapting
to weightless and virtual environments. J Vestib Res 2:307–322
9. Wang Y, Rahmatalla S (2013) Human head-neck models in whole-body vibration: effect of
posture. J Biomech 46(4):702–710
10. Cesarani A, Alpini D, Barozzi S (1990) Electrical stimulation in the treatment of acute vertigo.
In: Sacristan T, Alvarez-Vincent JJ, Bartual J, Antoli-Candela F (eds) Otorhinolaryngology,
head & neck surgery. Proceedings of the XIV World Congress of Otorhinolaryngology,
Madrid, 1989. Kugler & Ghedini Publ, Amsterdam/Berkeley/Milano
11. Cesarani A, Alpini D, Barozzi S (1990) Neck electrical stimulation in the treatment of laby-
rinth acute vertigo. Riv Ital EEG Neurof Clin 13(1):55–61
12. Cesarani A, Pertoni T, Alpini D (1988) L’electrostimulation cervicale posteriore dans la reha-
bilitation des handicaps vestibulaires. XXII Reunion de la Societe d’otoneurologie de Langue
Francaise, Toulose, May 1988
13. Cesarani A, Alpini D, Barozzi S (1989) L’electrostimulation electrique dans la reeducation
vestibulaire: indications, limites, perspectives. XXIII Reunion de la Societe d’Otoneurologie
de Langue Francaise, Modena, June 1989
14. Cesarani A, Alpini D (1991) New trends in rehabilitation treatment of vertigo and dizziness.
In: Akyildiz N, Portmann M (eds) Vertigo and its treatment. Proceedings of international sym-
posium for Prof G Portmann’s Centenary, Ankara, 16–18 Maggio 1990, pp 90–104
15. Cesarani A, Alpini D, Barozzi S (1992) Superficial paravertebral electrical stimulation. A con-
servative treatment of vertigo and dizziness. In: Claussen CF, Kirtane MV, Schneider D (eds)
Conservative versus surgical treatment of sensorineural hearing loss, tinnitus, vertigo and nausea.
Proceedings of the XVIII NES Congress, Dr Werner Rudat & Co, Nach. edi, m + p, Hamburg
16. Cesarani A, Alpini D, Barozzi S, Osio M (1993) Superficial paravertebral electrical stimulation
(SPES) in the treatment of vertigo and disequilibrium disturbances. In: Dufour A (ed)
Proceedings XXVII symposium Societe d’Oto-Neurologie de Langue Francaise Sanremo, p 47
17. Cesarani A (1994) The cervical electrostimulation. Neurootol Newslett 1(1):67–72
18. Alpini D, Cesarani A, Barozzi S (1992) Non pharmacological treatment of acute vertigo. In:
Claussen CF, Kirtane MV, Schneider D (eds) Diagnostic procedures and imaging techniques
used in neurotology. Proceedings of the XVI NES Congress, Dr Werner Rudat & Co, Nachf
ed, m + p, Hamburg, pp 337–34018
19. Tseng CC, Wang SJ, Young YH (2013) Comparison of head elevation versus rotation methods
for eliciting cervical vestibular-evoked myogenic potentials via bone-conducted vibration. Int
J Audiol 52(3):200–206
The Neurophysiological Basis
of Vestibular Electrical Stimulation 31
M. Osio, L. Brunati, G. Abello, and A. Mangoni
31.1 Introduction
Bending the neck and turning the head respecting to the body cause the stimulation
of the cervical proprioceptors. This kind of receptors activates a pathway projecting
to the vestibular nuclei.
The impulses are reflected through the nucleo-reticular formation and then to the
spinal cord. Such activation allows movements of the neck to influence the postural
set and to modify the activation of the antigravity muscles of the lower limbs.
This pattern of muscular activation is hypnotized on the basis of the so-called
neck-postural reflexes, or better named cervico-spinal reflex [1]. During the con-
traction of the paravertebral muscles of the neck, there is a response characterized
by inhibition of ipsilateral soleus in respect to the side of neck stimulation and
facilitation of the contralateral muscles [2, 3]. During the superficial electrical stim-
ulation (SES), the paraspinal muscles are also activated and there are previous stud-
ies that show that SES is able to reduce vertigo and dizziness [4]. This kind of
stimulation is also able to evoke changes in activity of the muscles of the legs. We
used a neurophysiological test named H-reflex to control this modification. It holds
special interest because it can attest the activation of the vestibular-spinal way dur-
ing the stimulation of the paraspinal muscles through the modification of excitabil-
ity of the motoneuron. Under appropriate conditions, a single electrical shock to the
tibial nerve will evoke two discrete motor action potentials in the calf muscles. The
M. Osio (*) • A. Mangoni

Department of Neurology, Neurophysiology “Sacco” Hospital,
Via G.B. Grassi, 74, 20157, Milano, Italy
e-mail: osio.maurizio@hsacco.it
L. Brunati
“Pro Juventute” Foundation, IRCCS “Don Carlo Gnocchi” Foundation,
Via Capecelatro 66, 2100, Milan, Italy
G. Abello
Bioengineering Department, Politecnico di Milano, Via C. Golgi, 39, 20133, Milano, Italy

322 M. Osio et al.
first potential, the M-wave, results from direct stimulation of motor nerve fibers.
The second potential, the H-wave, is the expression of a monosynaptic reflex, which
runs in afferent fibers (I1 a) from the neuromuscular spindles and back again through
motor afferents. Since no interneurons are involved, the size of the second action
potential will provide a measure of motoneuron excitability under a variety of
experimental conditions [5, 6].
31.2 Material and Methods
Eight normal subjects (5 females and 3 males), aged between 20 and 33 years old,
were admitted to the study. Subject did all sit in a comfortable armchair, with cervi-
cal spine at rest position with non-flexion, extension, or lateral bending and head
support and not rotated with respect to the trunk.
Legs were at rest and supported, the hips were flexed at 90°, the knees were
flexed at 120°, and the ankles were flexed at 90°. Patients were in a quiet room and
were awake and relaxed with eyes closed.
Recording of the H-reflex was obtained with pregelled surface electrodes.
Active electrode was fixed on the distal on the belly of soleus muscle, while refer-
ence electrode was fixed 30 mm below. Stimulation of the tibial nerve was per-
formed with surface electrodes at the popliteal fossa. Interelectrodes distance was
25 mm. Stimulus duration was 1 ms. All this is in accordance with the indication
of the literature [5]. Stimulus intensity was between 5 and 21 mA at the intensity
needed to evoke the maximum amplitude of the H-reflex (H Max) for each
subject.
H Max from soleus muscle right and left legs was recorded every 5 min before,
during, and after the stimulation of the muscles. In particular superficial electrical
stimulation (SES) of neck paravertebral muscles and contemporary contralateral
upper part of the trapezius was applied. SES of the neck muscles was applied with
pulse rate of 80 Hz and a pulse width randomly modulated between 100 and 200 ps
of duration (so-called vestibular electrical stimulation – VES – see Chap. 30). First
VES application was performed for 15 min contemporaneously on the right para-
vertebral muscles of the neck and on the left upper part of trapezius muscle. After
30 min VES was applied to the contralateral paravertebral of the neck and trapezius
muscle for a duration of 15 min. The recordings of the H Max were obtained by left
and right leg. We calculated mean (M) and standard deviation (SD) of the five con-
secutive H Max responses, and obtained values were tabulated. Measures of H Max
value were done every 5 min. For each subject were recorded one H Max basal
value before application VES, 3 H Max were obtained every 5 min during VES
applied to the right paravertebral and left trapezius muscle; 3–6 H Max during to
recovery phase, 1 H Max basal, 3 H Max values during VES applied to the left
paravertebral muscle and right trapezius muscle, and 3–6 H Max values obtained
during a second recovery phase. Statistical analysis was performed with the
Student’s t-test comparing H Max recorded before, during, and after each VES
application.
31 The Neurophysiological Basis of Vestibular Electrical Stimulation 323
SES: left paravertebrals − right trapezius

H Max changes
H Max %
140
p = 0.02
Right soleus
120
100
80
Left soleus
p = 0.01
60 p = 0.01
Stimulation
40
0 5 10 15 20 25
min
n=8
Fig. 31.1 Effects of electrical stimulation on H-reflexes
31.3 Results
They were homogeneous in all subjects both for the stimulation patterns.
The contemporary VES of the left paravertebral cervical muscles and of the right
trapezius was enhanced in all subjects after 10 min, H Max amplitude (14 % of the
maximum amplitude; p = 0.02) of the right soleus muscle, and reduced after 15 min,
H Max amplitude (−20 %; p = 0.001) of the soleus muscles. H Max amplitude
returned to the basal values 10 min after the end of the stimulation on the right
soleus and was still reduced (−36 %; p = 0.001) 10 min after the end of SES on the
left soleus. In some subjects H Max values lasted less than normal for 30 min after
the end of VES. Recording from the right soleus showed that 10 min after the end
of VES amplitude was still decreased (27 %; p = 0.001) in some subject inhibition
of the H-reflex that lasted over 30 min (Fig. 31.1).
The stimulation by VES of the right paravertebral cervical muscles and left
trapezius induced, after 5 min, an increase of the left side values (20 %; p = 0.001)
and reduced, after 15 min, the amplitude of the right values (−32 %; p = 0.001).
In a short time after the end of the SES, left H-reflex returns to basal values.
When a paradoxal second phase begins, H-reflex decreases slowly but progres-
sively reaching a new “basal” value that is significantly (p = 0.001) lower. Right
H-reflex remains reduced at least 10 min after the end of SES (−27 %; p = 0.001)
(Fig. 31.2).
324 M. Osio et al.
SES: left paravertebrals − left trapezius

H Max changes
H Max %
140
p = 0.01
Left soleus
120
100
p = 0.01
80
p = 0.01
Right soleus
p = 0.01
60
Stimulation
40
0 5 10 15 20 25
min
n=8
Fig. 31.2 Effects of electrical stimulation on H-reflexes
Conclusions
The results of the present study showed that VES of the neck muscles clearly
influenced the excitability of the motor neurons of the lower limbs.
It is important to underline that VES at the intensity to which was applied
never evoked muscles contraction. On the contrary VES was applied in the same
frequency range (80 Hz) which is able to activate muscles spindles by vibratory
stimulation. Thus, it is likely that VES activate the same spinal pathways acti-
vated from the cervico-spinal reflexes, modulating in the same way the postural
reflexes of the lower limbs. This action is probably mediated from proprioceptive
input originated in the spindles of the neck muscles [7]. Otherwise we cannot
exclude the action of skin receptors mediating the vibratory sense.
Proprioceptive afferent input evoked from VES of the neck muscles could
reach also contralateral Deiters vestibular nuclei and cortex, probably by mean of
reticular pathways. In such way SES may influence the equilibrium system. It is
known [8] that if vestibular apparatus is damaged, the reflexes of the neck, limb,
and eyes muscles become prominent. Therefore it is possible that VES action in
treatment of vertigo and dizziness is based on the modulation of the propriocep-
tive input from neck muscles.
At last there is the observation that inhibitory effect is more pronounced and
long lasting than the excitatory one. Supraspinal pathway activation [9] may give
account of this phenomenon, but further investigations are needed to verify such
hypothesis.
31 The Neurophysiological Basis of Vestibular Electrical Stimulation 325
References
1. Ghez C (1991) Posture. In: Kaendel ER, Schwartz JH, Jessell TM (eds) Principles of neural
sciences, 3rd edn. Elsevier, New York/Amsterdam/London/Tokyo, pp 596–607
2. Angel RW, Hofmann WW (1963) The H reflex in normal, spastic and rigid subjects. Arch
Neurol 8:591–596
3. YaM K (1979) The organization of voluntary movement. Neurophysiological mechanisms, vol
II. Plenum Press, New York/London, pp 27–503
4. Alpini D, Cesarani A, Barozzi S (1992) Non pharmacological treatment of acute vertigo. In:
Claussen CF, Kirtane MV, Schneider D (eds) Diagnostic procedures and imagining techniques
used in neurotology. Proceedings of the XVI NES Congress. Werner Rudat & Co, Nachf ed
m + p, Hamburg, pp 337–340
5. Thompson AK, Chen XY, Wolpaw JR (2013) Soleus H-reflex operant conditioning changes the
H-reflex recruitment curve. Muscle Nerve 47(4):539–544
6. Oliveira MI, Machado AR, Chagas VG, Granado TC, Pereira AA, Andrade AO (2012) On the
use of evoked potentials for quantification of pain. Conf Proc IEEE Eng Med Biol Soc
2012:1578–1581
7. Shields RK, Dudley-Javoroski S (2013) Fatigue modulates synchronous but not asynchronous
soleus activation during stimulation of paralyzed muscle. Clin Neurophysiol
11:S1388-2457(13)00278-2
8. Okuma Y, Bergquist AJ, Hong M, Chan KM, Collins DF (2013) Electrical stimulation site
influences the spatial distribution of motor units recruited in tibialis anterior. Clin Neurophysiol
18: S1388-2457(13)00315-5
9. Lagerquist O, Mang CS, Collins DF (2012) Changes in spinal but not cortical excitability fol-
lowing combined electrical stimulation of the tibial nerve and voluntary plantar-flexion. Exp
Brain Res 222(1–2):41–53
Ski Trainer Oscillating Platform:
Proprioceptive Reeducation 32
M. Savini, D.C. Alpini, and A. Cesarani
32.1 Introduction
Reeducation of the proprioceptive reflexes is especially indicated in posttraumatic

disequilibrium. This method uses the theoretical premises of the method known as
“proprioceptive neuromuscular facilitation” by (1) the use of nervous information
of surface origin (tactile data) and (2) coordination of the information of deep origin
(joint place, stretching of tendons, and capsuloligamentous complexes).
This peripheral information stimulates the nervous system, which triggers the
muscle. In this way the patient may relearn to balance on his foot or knee via reco-
ordination of the reflexes in unstable positions. He thus learns progressively to
admit and understand the unstableness after an accident and is guided to fight
against this residual unstableness through an improved muscular interplay [1, 2].
Skitter is a ski trainer platform comprised of an oscillating plate on which two
foot pads are placed. Each foot pad is able to move anteroposteriorly (toes up and
toes down) and lateral senses also allow torsional movement of each foot. The plate
on which the two foot pads are placed is able to surf on an oscillating small table
(Fig. 32.1a).
The oscillations of the table are slowed by elastic cords that regulate the resis-
tance with which the device opposes the patient’s movements. These movements of
M. Savini
Istituto Clinico Città Studi, via Jommelli 17, Milan, Italy
D.C. Alpini (*)
ENT-Otoneurology Service, IRCCS “Don Carlo C. Gnocchi” Foundation, Milano, Italy
A. Cesarani
University of Milan, Milano, Italy
Audiology Unit, IRCCS “Ca’ Granda” Ospedale Maggiore Policlinico, Milano, Italy

328 M. Savini et al.
Fig. 32.1 Skitter (a) and a

skier (b)
a b
Fig. 32.2 Forward (a) and backward (b) leg extensions
the feet and, especially, surfing and oscillating of the body simulate the movements
performed during skiing (Fig. 32.1b).
We usually employed Skitter for proprioceptive reeducation of posttraumatic
unsteadiness and dizziness because it allows the use of cognitively involved exer-
cises and improvement of sensorial coordination when visual feedback is
32 Ski Trainer Oscillating Platform: Proprioceptive Reeducation 329
a b
Fig. 32.3 Ankle-hip lateral strategies (a) and with oscillations (b)
associated in order to improve head-to-trunk dynamic stabilization [3]. To success-

fully reeducate reflexes by this method, active cooperation of the subject is needed.
The careful activity of a reeducator or of a physiotherapist offers better chances of
success [4].
In whiplash patients we standardized a protocol that has been used in patients
ranging from 18 to 45 years of age. According to the obvious limits of age, Skitter
can be employed (with the constant help of the reeducator) also in older subjects,
but usually it is not possible to perform the entire protocol. To achieve a good result,
it is crucial that the articulations of ankle, knee, and hip are complete and that the
muscular tone, especially of the thigh, is good. Sometimes previous tonification of
the muscles is in fact necessary before starting reeducation of the proprioceptive
reflexes.
32.1.1 Forward Leg Extensions (Fig. 32.2a)
1. With one foot on the end cap and the other across the foot pad, the patient keeps
his weight forward and extends the front leg in a controlled manner, then he
returns slowly and repeats. It improves quads and trunk muscles and stabilizes
ankles and knees.
2. The patient maintains the leg extension position, and the therapist destabilizes
him by moving the platform during visual fixation of a point.
3. The patient performs a leg extension with closed eyes to improve self-perception
of muscle tone.
32.1.2 Backward Leg Extensions (Fig. 32.2b)
This is similar to forward leg extensions except the focus is on the rear leg. With a
stable, controlled movement, the patient extends the leg back to the end and repeats
on both legs. It improves gluts and quads, hamstrings, and trunk muscles, and stabi-
lizes ankles and knees.
According to the neuro-otologic and equilibriometric characteristics of the
patient, leg extensions should be performed for both legs or only for one leg.
32.1.3 Ankle-Hip Strategies (Fig. 32.3a)
The patient steps on the foot pads with feet centrally positioned. Then he concen-
trates on proper posture using a mirror to see his reflection and transfers his weight
from one foot to the other with a smooth flowing motion.
During this smooth and rhythmic weight transfer, the therapist induces body
movements according to ankle or hip strategies.
32.1.4 Visual Feedback
The patient is comfortably stable on the foot pads. With his thumbs and extended
limbs, he tries to touch some visual targets placed in different positions on a mirror
in front of him.
32.1.5 Oscillations (Fig. 32.3b)
The patient steps on foot pads with feet centrally positioned. Then he concentrates
on proper posture using a mirror to see his reflection. With eyes closed he transfers
his weight from one foot to the other with a smooth flowing motion. During this
smooth and rhythmic weight transfer, the therapist pushes the bumpers at one end
of the Skitter inducing a sudden and unpredictable inclination of the device.
32.1.6 One Leg
The patient maintains equilibrium on one leg with the other extended (Fig. 32.4a) or
flexed (Fig. 32.4b) or with one leg lateral (Fig. 32.5). The therapist helps the patient
either to maintain equilibrium or to correct his posture. A mirror facilitates postural
equilibrium strategies correction.
32.1.7 Slalom (Fig. 32.6)
The patient steps on the foot pads with feet centrally positioned. Then he concen-
trates on proper posture using a mirror to see his reflection and begins to transfer
his weight from one foot to the other with a smooth flowing motion. As his rhythms
32 Ski Trainer Oscillating Platform: Proprioceptive Reeducation 331
a b
Fig. 32.4 Extended (a) or flexed (b) exercises with one leg
Fig. 32.5 One-leg exercise
increase he will get closer to the bumpers at each end, always maintaining good
upright posture with eyes focused in the mirror and paying attention to his balance.
If the exercise is performed with limited upper body movement (such as in slalom),
it improves hip rotators, quads, and calves, while it stimulates abdominal stabiliz-
ers and gluts when the patient includes upper body motion (such as in giant sla-
lom). Exercises have to be performed concentrating on proper edge setting
techniques.
Fig. 32.6 Slalom exercise
32.1.8 Ankles Stability
The patient keeps his knees straight pushing the skate forward with his toes and
pulling back with his heels. He has to concentrate on using only the ankles and
calves, while all the other muscles are relaxed. It improves calves and ankle stability
and balance proprioception.
References
1. Corna S, Nardone A, Prestinari A, Galante M, Grasso M, Schieppati M (2003) Comparison of
Cawthorne-Cooksey exercises and sinusoidal support surface translations to improve balance
in patients with unilateral vestibular deficit. Arch Phys Med Rehabil 84(8):1173–1184
2. Nardone A, Godi M, Artuso A, Schieppati M (2010) Balance rehabilitation by moving plat-
form and exercises in patients with neuropathy or vestibular deficit. Arch Phys Med Rehabil
91(12):1869–1877
3. De Nunzio AM, Nardone A, Schieppati M (2005) Head stabilization on a continuously oscil-
lating platform: the effect of a proprioceptive disturbance on the balancing strategy. Exp Brain
Res 165(2):261–272
4. Fairburn PS, Palmer R, Whybrow J, Fielden S, Jones S (2000) A prototype system for testing
force platform dynamic performance. Gait Posture 12(1):25–33
Visual Feedback Postural
Control Re-education 33
D.C. Alpini, A. Cesarani, M. De Bellis,
R. Kohen-Raz, and D. Riva
33.1 Introduction
Maintaining postural stability is a complex process [1] involving the coordinated

actions of biomechanical, sensory, motor, and central nervous system components.
A relatively simple biomechanical definition for postural stability can be formulated
in terms of the position of the body center of gravity relative to the base of support.
The body movements used to maintain postural stability, however, are complex
because of the number of joint systems and muscles involved. The center of gravity
(CoG) is the point at which the whole weight of a body may be considered to act. In
humans who are standing quietly and vertically erect, the CoG is located at the level
of the hips and slightly forward of the ankle joints. CoG height is 0.5527 of total
height. CoG and center of mass (CoM) are equivalent points in space when the
gravitational field is uniform and gravity is the only force under consideration.
Shumway-Cook et al. [2] conducted the first study that used objective visual
feedback (VFB), based on symmetry of postural sway (movement of the CoG), for
training purposes.
D.C. Alpini (*)

A. Cesarani
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
M. De Bellis
ENT Department, Desio Hospital (Mi), Milan, Italy
R. Kohen-Raz
The school of Education, The Hebrew University of Jerusalem, Har ha-Tsofim, Jerusalem, Israel
D. Riva
International Society of Proprioception and Posture, via Valgioie 87, 10146 Torino, Italy

Nowadays, a lot of different posturographic equipments are available and VFB is

frequently used to improve postural stability control.
For the scope of the chapter, even if nowadays for postural visual feedback reha-
bilitation [3–5], examples are based on the Balance Master System (Neurocom,
Clackamas, OR, USA, http://resourceonbalance.com), Tetrax FB System (Tel Aviv
Israel, www.tetraxfb.com), and the Delos System (Turin, Italy, www.delos-
international.com).
Balance Master is an equipment that allows, by means of a dual footplate, a
visual feedback of CoG position, projected on a computer screen facing the patient
standing on the platform [6–8] (see also Chap. 15).
Tetrax system is based on recording of separate CoG of the anterior and posterior
part of the 2 ft [9–16] (see also Chap. 15).
Delos System is an equipment constituted by a unstable and oscillating platform
and two accelerometers, one on the trunk [17] and one on the head (see also Chap.
16). In this way the visual feedback projected on the screen may regard the move-
ments of the table or the trunk or the head or a combination of the three.
33.2 Balance Master
When normal subjects maintain a vertically erect position, the CoG is located
directly over the area of the feet support, slightly forward of the ankle joints. This
position can be maintained without stepping or reaching for support if sway does
not exceed the subject’s limits of stability (Fig. 33.1).
Functional stability limits (limits of stability, LoS) have been calculated to be
6.25″ anteriorly and 4.45″ posteriorly for the average adult subject. The angular
limits of stability are very nearly the same for all adults regardless of height. The
biomechanical properties that determine the LoS are similar for standing in place,
walking, and sitting without trunk support. For these reasons reeducation of the
limits of stability in standing in place can be used to rehabilitate the patient to regain
normal LoS during walking, too.
LoS test and exercise require the subject to be able to actively move his/her CoG
away from the center toward a visual target and maintain that position for the
required time. The correct execution of the LoS test requires normal combined and
integrated ankle-hip strategies (Fig. 33.2).
LoS parameters to be considered are:
Movement time, how many seconds the patient takes to reach the desired target
(including the reaction time).
Path sway, that refers percentage of path length.
Target sway, percentage of maximum CoG area maintained on the target.
Patient position, value given in polar coordinates that represents the average position of
the COG during the period of target sway assessment. If the target was not reached,
the patient position score reflects the point of closest approach to the target.
Distance error, difference between the patient’s average position and the center of
target. This parameter allows one to see how far away from the center the patient
is willing and able to move in a given direction.
33 Visual Feedback Postural Control Re-education 335
Fig. 33.1 Balance Master

equipment
LoS misperception is common findings in whiplash patients. In these cases train-

ing aimed at teaching the appropriate conditions for using ankle movements can
have a positive impact. In contrast, weakness of ankle joint muscles, loss of ankle
sensation, reduced mobility about the ankles, or combinations of these factors pre-
vent the patient from generating effective ankle movements and might be an abnor-
mal adaptation used by a dizzy patient to minimize head movements and associated
stimulation of the neck and vestibular system.
By means of the Balance Master it is possible to treat patients ranging from 76 to
203 cm in height and from 18 to 138 kg in weight. Each treatment session can be
performed according to the LoS, ranging from 25 to 100 % of the predictable LoS,
in 5 % increments. The target pacing is 1, 3, 5, 7, 10, 15, and 20 s. If trying to pro-
mote faster movement, then low pacing settings (1, 2, 5 s) are appropriate. If stabil-
ity at points in space is desired, then higher pacing settings (10 s or higher) are
appropriate so that the patient must “hold” a position (Fig. 33.3).
The duration of each session treatment is 20 min. The frequency generally varies
from twice a week to every day treatment. The frequency of training sessions is
dependent on a combination of other rehabilitative treatments such as physical
therapy and vestibular electrical stimulation.
PATIENT INFORMATION AND TEST SETTINGS

Patient Name: Age: 30 Test Date. 02/16/95
Data file Ht.: 172 cm Order #: 6
Target/prot. Type: SP06 LOS: 75 %
Therapy Mode: Beep, Feedback Pacing Speed: 10 sec
Post-Test Comment:
Limits of stability
PATH SWAY AREA

Numeric Summary
Mvt Path Target Patient Distance Direction
Time Sway Sway Position Error Error
Transition (sec) (% Path Len) (% Max Area) (% LOS) (deg) (% LOS) (deg)
1 (F) 4.28 127.68 N/S <72.1> <359.2> <–2.9> <–0.8>
2 (RF) 4.00 172.16 0.41 70.8 42.7 –4.2 –2.3
3 (R) 4.04 157.96 N/S <71.8> <87.8> <–3.2> <–2.2>
4 (RB) 2.94 169.83 0.58 68.6 124.8 –6.4 –10.2
5 (B) 3.74 237.19 0.13 66.8 176.6 –8.2 –3.4
6 (LB) 6.72 347.19 N/S <60.6> <230.8> <–14.4> <–5.8>
7 (L) 4.50 188.06 N/S <73.4> <271.9> <–1.6> <1.9>
8 (LF) 3.70 158.90 0.20 70.1 314.2 –4.9 –0.8
Fig. 33.2 Example of LoS, a not completely statistical representation
33.2.1 Tetrax FB
Tetrax FB works within the principles of Simplexity [18], which state that a human
body’s balance in space is based on the cooperation and interaction of a multiplicity
and complexity of many subsystems which are under the control of efficient neuro-
physiological mechanisms. It consists of four independent mobile force plates, two
for each foot. Each plate contains a strain-gauge force transducer, which is sensitive
to vertical force. Tetrax provides independent output from the four balance plates.
Subjects are requested to stand quietly on the platforms and control CoG displace-
ments using both feet, toes, and heels in a synchronized and coordinated way. “Tetra
CoG” have to be moved along visual presented pathways (e.g., a labyrinth, Fig. 33.3)
as correctly as possible (Fig. 33.4).
The pressure fluctuations produced by the heels and toes of a subject standing
with different positions of the trunk or the head may be visually balanced through
the feedback presented on the screen.
No ST1 Ctr/ ST3 Ant/ ST11 Ctr/ ST19

Target Ant Post 3Ant
Align ST2 Ctr/ ST4 LLat/ ST12 Ctr/ ST20

Ctr RAnt RLat 3R
Ctr/ ST5 Rant/ ST13 Ctrl/ ST21

RLat LPost 3Post
Ctr/ ST6 LAnt/ ST14 Ctr/ ST22

RPost RPost 3L
Ctr/ ST7 LAnt/ ST15 Circle ST23

Post RAnt R
Ctr/ ST8 RAnt/ ST16 Circle ST24

LPost RPost L
Ctr/ ST9 LPost/ ST17 ST25

Ctr/
LLat RPost Ant/
Post
Ctr/ ST10 LAnt/ ST18 Ctr/ RLat

LAnt LPost LLat
Standard Targets
Fig. 33.3 Standard targets available for treatment

Fig. 33.4 Tetrax FB

equipment
33.2.2 Delos
It is based on an electronic rocking board, with “a degree of freedom” and visual

tracking of the micro-rolling of the point of support. Its exclusive rocking move-
ment, combined with the subcortical visual tracking in real time, creates conditions
of instability capable of activating high-frequency proprioceptive flows both in
standing (Fig. 33.5) and sitting position (Fig. 33.6).
The rolling surfaces with variable radius permit the proposal of different levels
of instability and the selective activation of the postural strategies. The postural
reader measures the subject’s levels of stability in static and dynamic, monopo-
dalic, bipodalic, and seated conditions. It records and visualizes in real time the
movements on the frontal and sagittal planes in relation to the vertical axis. The
system may use also a wireless electronic rocking board with “3 degrees of free-
dom” with visualization in real time of the movements on the x-, y-, and z-axis.
Tridimensional view of the trials represents the completion of DEB2 proposal,
widening the number of biomechanical and postural situations to be managed.
The rolling surfaces with variable radius permit the proposal of increasing levels
of instability.
Figs. 33.5 and 33.6 Delos

DEB 2 equipment comprising
the electronic rocking board
and the two accelerometers
on the head and the trunk
Figs. 33.5
and 33.6 (continued)
Conclusions
VFB provides a ready source of information about postural instability for both
the patient and the therapist. The purpose of VFB is to detect and make available
to the patient objective information about physiological function or movement
that is not ordinarily perceived by the patient (e.g., Balance Master).
In the case of postural instability caused by whiplash injuries, visual and audi-
tory (beep) signals have been used to give the patient information about head and
trunk orientation (e.g., Delos) and about symmetry of weight bearing through the
lower extremities (e.g., Tetrax). The assumption is that the patient can use visual
or auditory cues better than he or she could use somatosensory or vestibular
inputs.
For the therapist the VFB facilitates the design of custom treatments, and for
the patient it enhances motivation through real-time visual feedback, links per-
ception to movement, internalizes the appropriate alignment or movement pat-
tern, improves volitional control, and builds confidence to perform activities of
daily living.
Recently it has been proposed the use of Nintendo Wii, a popular virtual real-
ity (VR) video gaming system, both as physiotherapist-assisted [19] and home-
based [20] exercises.
Nintendo Wii Balance Board is cost-effective and user-friendly [21] and has
been proposed as an alternative to other popular frequently used systems in
elderly patients [22], but it is limited in its customizability to accommodate dif-
ferent functional levels, thus in our experience, professional equipments have to
be preferred for WAD rehabilitation.
References
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gravity. Electroenceph Clin Neurophysiol 76:165–176
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and practical application, & physical therapy. Chattanooga Corp, Chattanooga, pp 123–138
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on human head movement and postural patterns during stance. J Vest Res 3:409–417
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Clinical exercise physiology. Mosby, St Louis, p 57
7. Neurocom International Inc. (1989) Balance master operator’s manual. Neurocom, Portland
8. Daleiden S (1990) Weight shifting as a treatment for balance deficits. A literature review.
Physiother Can 48:81–87
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mobility related accidents in elderly and disabled. Proceedings of the 3rd international confer-
ence on disability, virtual reality and ass. Tech., Alghero, Italy, pp 249–254
10. Himmelfarb R, Kohen-Raz R, Rapaport J, Bloom A (1992) The application of posturography
in the assessment of vertiginous disorders caused by head and neck injuries. Proceedings of he
international meeting on whiplash injuries. University of Wales, Wales
11. Kohen-Raz R, Gentaz R (1993) Posturographic characteristics of patients with lower back
pain. Cahiers de Posturologie, Paris
12. Kohen-Raz R (1986) Learning disabilities and postural control. Freund Publishing House, Tel
Aviv
13. Kohen-Raz R, Roth V (1998) Posturographic characteristics of Whiplash patients. Proceedings
of the XII regular meeting of the Barany Society, Wuerzburg, Germany. In: Claus CF, Claus-
Toni H, Hoffenberth B (eds) Equilibrium research, Clinical equilibriometry and modern treat-
ment. Elsevier, Amsterdam, 2000
14. Roth V, Perlson Y (1997) The contribution of an interactive balance recording system (IBS) to
the diagnosis, treatment and follow up of Foot and Ankle Injuries. Proceedings of the interna-
tional congress on foot and ankle injuries, Jerusalem, January 1997
15. Turner D (1998) Evaluation of the tetrax interactive balance system and equitest using normal
subjects. MSc thesis, University of Southampton
16. Lee KG, Chun MH, Kang SH, Kim BR (2008) The evaluation of effect after biofeedback train-
ing using interactive balance system in sub-acute stroke patients. Asan Medical Center Korea,
XVII. European stroke conference Nice, France. Poster Session: Recovery and rehabilitation,
May 2008
18. Berthoz A (2012) Simplexity. Yale University Press, London
19. Levac DE, Miller PA (2013) Integrating virtual reality video games into practice: clinicians’
experiences. Physiother Theory Pract;29(7):504–512
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Neurorehabilitation of Ataxia
34
M. Forni
34.1 Introduction
The meaning of ataxia is failure of coordination. Ataxic patients are not able to
define the width, velocity, and rhythms of muscle contractions and cannot coordi-
nate more muscle groups which are synchronously activated. The ataxia can be
determined by (1) injury of the proprioceptive afferences, (2) labyrinthic injury, and
(3) injury of cerebellum or its connections which are reciprocally connected to the
cerebral cortex (neocerebellum), the spinal cord (paleocerebellum), and the vestibu-
lar system (archeocerebellum).
Post-whiplash ataxia is not frequent and it attains to polytrauma patients. The
walking ataxia – often generically considered as walking balance disease – can also
be generated by an injury of the pyramidal paths causing a heavy recruitment deficit
of the lower limb proximal areas. We use the word “ataxia” with the meaning of
coordination and motor control alteration due to the inability of the antagonistic
muscle couples to synergistically operate. It can occur as postural instability of one
or more body segments or as dyssynergia when holding a posture during the execu-
tion of a complex motion [1, 2]. Ataxia can be often found in whiplash-type injuries
and sometimes in the acute phase shows reversibility, probably because it is sup-
ported by a simple neuro-apraxia of the corresponding nervous paths. In cases in
which the ataxia is present with instability, it is usually supported by injuries of the
direct or indirect proprioceptive paths or the cerebellospinal paths flowing to the
cervical spinal cord. From the functional point of view, ataxia can be defined as a
specific difficulty in controlling the center of gravity of the whole body or of single
articulated segments. In fact, it magically disappears when the patient is immersed
into water [3].
M. Forni
Rehabilitation Unit, IRCCS “Don Carlo Gnocchi” Foundation,
Marina di Massa (MS), Italy
e-mail: mforni@dongnocchi.it

344 M. Forni
34.1.1 Treatment Outlines
If considered on the plane of a system which can be influenced by therapeutic

exercise, that is, on the interface between environment and spinal segmentary sys-
tems (receptor level and muscle effector level), ataxia can be defined as the inability
to couple suitably coactivation and reciprocal activation, the latter the pathologi-
cally prevalent characteristic. From the spinal cord point of view, in fact, hypotonia
could be considered as the cause of the ataxia. In fact, if we consider ataxia as
increase of the stretching reflex threshold due to decreasing of the fusi basal dis-
charge, we can formulate the hypothesis that the motion desynchronization is sup-
ported by a decreasing of the tonic “brake,” due to perceptive distortions connected
to the proprioceptor-altered operation. Further, we could consider ataxia as the
extreme pole of a continuous path with variable prevalence grades between coacti-
vation and reciprocal activation, in which the opposite is spasticity. In fact, correct
motion requires a rigidity entity which is able to withstand stimuli or a flexibility
that is the ability to follow stimuli. Ataxia can be considered as an excessive flexi-
bility. The posturogram of a normal person is known to often show variability in the
center of gravity displacement, which is the expression of physiological flexibility.
The motion pre-patterns, that is, the anticipatory muscle activation of an intentional
motion being carried out, are one of the physiological examples of the control of
this CNS variability. The therapeutic approach to ataxia cannot be separated from
such considerations [4]. The most important problem in the spontaneous adaptation
to the symptom in the atactic patient is normally that the spontaneous reaction
increases the symptom.
The “body’s intelligence” reacts against the instability by increasing the rigidity,
that is, the cocontraction, which is the real mechanism altered by the pathology.
This condition activates the paradoxical happening so that the instability increases
with the increasing of attempts aimed to limit it. Some preliminary therapeutical
results can be obtained simply by disconnecting this vicious circle by means of
relaxation techniques (which could be claimed as not suitable with regard to muscle
tone assessment), also of the psychomotor type. Taking into consideration that often
the whole spontaneous attempt of stopping the symptom accentuates it, the proposal
of “balance exercises” for the ataxic patient seems to be not justifiable. In fact, these
exercises are based on quick changes of the center of gravity, as imposed by the
rehabilitator, and are also based on the idea that after some stress of this type, an
adaptation should occur. It is my opinion that this adaptation – based on the idea that
the repetition is one of the mechanisms starting the process of learning – makes the
ataxia problem not solvable from the rehabilitation point of view.
An exercise plan for the ataxic patient should be based on a functional assess-
ment, recognizing the motion-specific characteristics as well as the necessary
changes needed to modify it. For example, we can examine whether the ataxic
motion is sensitive to inertial changes applied to the end of the considered segment
(weights), or to intentional changes (automatic-voluntary dissociation), or even
whether it uses any, and if so which, privileged afferent channels. Furthermore, the
description of the altered motion should include the planes on which the alteration
34 Neurorehabilitation of Ataxia 345
Table 34.1 Correlations between lesions and symptoms

Second-order
First-order lesion lesion
Lesion topography Functions Postural reactions associations associations
Efferent motor Pyramidal Inhibited
paths
Posterior cord Kinesthetic and Uncompleted, With synergically
afferent paths proprioceptive delayed reduced reactions
(deep sensory)
Cerebrocerebellar Neocerebellar Sequentially With
paths altered dissociated
reactions
Spinocerebellar Paleocerebellar Increased intensity With reactions
paths uninhibited in
direction and
intensity
Vestibulocerebellar Archeo-cerebellar Dynamically
paths displaced with
distal prevalence
Vestibulospinal Vestibular Statistically
paths distorted with
proximal
prevalence
is mainly evident as well as the articular angles and motion velocity at which the
motion is mainly compromised. Furthermore, we should examine whether the
motion is dynamically or statically altered.
The most interesting classification from the rehabilitation point of view is still P.
Gasco’s one [5], relevant to rehabilitation of motion in patients suffering from mul-
tiple sclerosis in its different expressions (Table 34.1).
Therefore we propose a descriptive assessment protocol to be associated, when
possible, with instrumental evaluations [1, 5]:
1. Assessment of ataxia “migration” in different body areas, with reference to pos-
ture; in fact, often the oscillation of one segment is complementary to and com-
pensates the adjacent segment oscillation and does not represent the injury site
from the topological point of view. The patient is evaluated in different postures
taking into consideration the syndrome’s acuteness: for example, in the erect
position (possibly also the monopodalic position), both with extended and flexed
knees, in a quadruped position, in crouched position, sitting down to exactly
examine the planes at which the motion is more compromised, and the postural
conditions in which the instability is evidenced in each body area. In the most
difficult cases, the patient can also be evaluated in a supine position thanks to
suitable supports, able to allow the cingulum to move with one or more degrees
of freedom.
2. Evaluation of synergies most stressed by the ataxia in the same body area [6].
Various modes of execution of the same action are evaluated (e.g., reaching to a
point in the space with one limb end or with the head or tracking of a trajectory
346 M. Forni
with one limb or the eyes, grasping of objects, reaching possible positions).
In this phase, the performance success or the execution correctness is not evalu-
ated, but the chosen “strategy,” above all on the basis of the degrees of freedom
or constraints imposed on the various segments implied or possible to be implied
in the motion.
3. Evaluation of the maximal voluntary cocontraction effects on the symptoms: the
patient is asked to try to actively stop the tremor or the postural instability by
stiffening as much as possible the involved segment and the adjacent segments.
Under the same other conditions, we note cases in which this operation is suc-
cessful and cases in which this operation causes instability or increasing
incoordination.
4. Evaluation of differences in the symptoms with respect to the voluntariness or
automatism of the motion; for example, in exercises with multiple conditions in
which an upper limb is laid on a moving plane and executes automatic support
functions, while the other limb executes an intentional job referred to a target
imposed by the examiner, then the operation of the examined limbs is inverted.
We note instability conditions which tend to occur more intentionally, than auto-
matically, and vice versa (considering the required cautions due to the kinesio-
logic differences between the two tasks).
5. Evaluation of differences in the symptoms [7] subsequent to segmentary motions
which are freely chosen by the patient, or segmentary motions imposed by the
examiner, but without perceptive guide, or motions with perceptive guide, such
as reaching a target or executing a trajectory following paths imposed by the
examiner.
6. Evaluation of the effect of suppression, increase, or distortion of one or more
perceptive channels (acoustic, visual, or proprioceptive) on the posture or
motion. The above six factors allow a functional assessment of the ataxia which
is more suitable than the traditional one used to plan therapy. In this way, the
therapeutic approach can be oriented to correction of the most specific aspects
which determine the incoordination or balance deficiency.
Naturally, this approach should be widened and validated, if possible, with
instrumental analysis able to control both the assessment correctness and the
efficiency of the therapeutic approach.
34.1.2 Treatment
Research evidence of activity-dependent central nervous system (CNS) plasticity

and the requisite motor learning principles can be used to construct an efficacious
motor recovery intervention. Brain plasticity after trauma refers to the regeneration
of brain neuronal structures and/or reorganization of the function of neurons. Not
only can CNS structure and function change in response to injury, but also the
changes may be modified by “activity.” For gait training or upper limb functional
training for stroke survivors, the “activity” is motor behavior, including coordina-
tion and strengthening exercise and functional training that comprise motor
learning. Critical principles of motor learning required for CNS activity-dependent

plasticity include close-to-normal movements, muscle activation driving practice of
movement, focused attention, repetition of desired movements, and training
specificity.
The ultimate goal of rehabilitation is to restore function so that a satisfying qual-
ity of life can be experienced.
Accurate measurement of dysfunction and its underlying impairments are criti-
cal to the development of accurately targeted interventions that are sufficiently
robust to produce gains not only in function but also in quality of life.
When it is not possible to adopt sophisticated instrumental evaluations, we think
it is very useful to monitor the condition with videotapes, which can be associated
with a functional assessment and allow one to have a relatively accurate idea about
the efficiency of the treatment. [7]
The International Classification of Functioning, Disability, and Health (ICF)
model of disablement, put forth by the World Health Organization, can provide not
only some guidance in measurement level selection but also can serve as a guide to
incorporate function and quality of life enhancement as the ultimate goals of reha-
bilitation interventions. Based on the evidence and principles of activity-dependent
plasticity and motor learning, we developed gait training and upper limb functional
training protocols.
An interesting perspective in ataxia therapy has been offered by the application
of “perceptive conflict” exercises for treatment of feedback control deficiency. This
approach, which can even use sophisticated methods such as virtual reality, is based
on the importance given in the determination of ataxia to the perceptive aspect and
to the possibility to restructure the balance system in the peripheral environment
through induced perceptive alterations.
Another interesting attempt is the use of an EMG-acoustic device able to monitor
muscular recruitment sequences in ballistic movements for treatment of prepro-
gramming level. In addition, the technique known as kinematic muscle shortening
with traction stress has also been successfully used. This method, based on motor
action organization theories – the best known of which is A. Feldman’s “equilib-
rium point” – is based on the possibility of recalling not present motion compo-
nents, shortening a muscle when contemporarily a vibration is applied to the muscle
itself (traction stress). In ataxia this exercise cannot be applied to all muscle groups;
in fact, the associated hypotonia implies that the strengthening reaction is recalled
at higher muscle lengths than the normal ones; sometime these lengths can exceed
the articular limits of the considered segment. The muscles on which the exercise
can be usually executed are short, generally phasic, muscle such as the posterior
neck muscles, to which the head is suspended in the vertical posture. This exercise
allowed us to obtain preliminary interesting results in head tremor control.
Other otoneurological techniques, almost of all which involve reflexologic
imprinting, are exhaustively described in other reports.
In many serious cases, it is possible to use technology to enable people with
ataxia to perform intended tasks such as feeding themselves. There are three ways
of reducing the effects of ataxia: (1) isolation from direct control, (2) modification
348 M. Forni
of feedback, and (3) mechanical loading for increasing inertia by adding a spring
with a definite stiffness, by adding mass, and by viscous damping. Many damped
orthoses have been created for many activities of daily living.
The ICF model suggests that we intervene at multiple lower levels (e.g., pathol-
ogy and impairment) in order to improve the higher levels of function and life role
participation. With the ICF model proffering the challenge of restoring life role
participation, it then becomes important to design and test interventions that result
in impairment gains sufficiently robust to be reflected in functional activities and
further in life role participation. Fortunately, CNS plasticity and associated motor
learning principles can serve well as the basis for generating such interventions.
These principles are useful in generating both efficacious gait training and effica-
cious upper limb functional training interventions. These principles also supported
incorporation of functional task practice and the demand of attention to task prac-
tice within the intervention. The ICF model provided the challenge to restore func-
tion and life role participation. The means to that end was provided by principles of
CNS plasticity and motor learning.
Despite multimodal intervention, persistence of tandem gait abnormality [8] is
particularly common.
Treadmill may be a useful tool to improve gait control in ataxic patients [9] with
possible gains in walking speed, Timed Up and Go, step length and balance, and
Rivermead Visual Gait Assessment. Freund and Stetts [10] to improve trunk stabi-
lization proposed a training and locomotor training (LT) using body-weight [11]
support on a treadmill (BWST). They reported improvement in movement, trans-
verse abdominis thickness, and isometric trunk [12] endurance tests after 10 weeks
of intervention.
Trunk control improvement has to be one of the main goal of posttraumatic
ataxia rehabilitation. In this way conventional [13] Bobath approach, also in its
“modern” reconceptualization [14, 15], seems to be still nowadays the best approach
to regain the ability to move selectively and the ability to produce coordinated
sequences of movement and vary movement patterns to fit a task, on the basis of
sensory input in motor behavior and learning.
Contemporary practice in the Bobath concept utilizes a problem-solving
approach to the individual’s clinical presentation and personal goals [16]. Treatment
is focused towards remediation, where possible, and guiding the individual towards
efficient movement strategies for task performance [17].
References
1. Dietz HC et al (1992) The coordination of posture and voluntary movement in patients with
cerebellar dysfunction. Mov Disord 7(1):14–22
2. Marsden CD (1975) The physiological basis of ataxia. Physiotherapy 61(11):326–328
3. Solari A, Filippini G, Gasco P, Colla L, Salmaggi A, La Mantia L, Farinotti M, Eoli M,
Mendozzi L (1999) Physical rehabilitation has a positive effect on disability in multiple sclero-
sis patients. Neurology 52(1):57–62
4. Grimaldi L et al (1986) Evocazione di componenti motorie assenti nelle lesioni del sistema
nervoso centrale. 11. Criteri di organizzazione degli atti motori. Giardini, Pisa
5. Gasco P (1994) La terapia riabilitativa dei pazienti con sclerosi multipla. In: Cazzullo CL et al
(eds) Sclerosi Multipla. Masson, Milano
6. Morgan MH et al (1975) Intention tremor-a method of measurement. J Neurol Neurosurg
Psychiatry 38:253–258
7. Sanes JN et a1. (1988) Visual and mechanical control of postural and kinetic tremor in cerebel-
lar system disorders. J Neurol Neurosurg Psychiat 51:934–9438; Daly JJ, Ruff RL (2007)
Construction of efficacious gait and upper limb functional interventions based on brain plastic-
ity evidence and model-based measures for stroke patients. Sci World J 7:2031–2345. doi:
10.1100/tsw.2007.299
8. Walker WC, Pickett TC (2007) Motor impairment after severe traumatic brain injury: A longi-
tudinal multicenter study. J Rehabil Res Dev 44(7):975–982
9. Vaz DV, Schettino Rde C, Rolla de Castro TR, Teixeira VR, Cavalcanti Furtado SR, de Mello
Figueiredo E (2008) Treadmill training for ataxic patients: a single-subject experimental
design. Clin Rehabil 22(3):234–241
10. Freund JE, Stetts DM (2010) Use of trunk stabilization and locomotor training in an adult with
cerebellar ataxia: a single system design. Physiother Theory Pract 26(7):447–458
11. Hewer RL et al (1972) An investigation into the value of treating intention tremor by weighting
the affected limb. Brain 95579–590
12. Michaelis J (1993) Mechanical methods of controlling ataxia. In: Bailliere’s (ed) Clinical neu-
rology. Bailliere’s Clinical Neurology 2(1): 121–139
13. Graham JV, Eustace C, Brock K, Swain E, Irwin-Carruthers S (2009) The Bobath concept in
contemporary clinical practice. Top Stroke Rehabil 16(1):57–68
14. Keser I, Kirdi N, Meric A, Kurne AT, Karabudak R (2013) Comparing routine neurorehabilita-
tion program with trunk exercises based on Bobath concept in multiple sclerosis: pilot study.
J Rehabil Res Dev 50(1):133–140
15. Karthikbabu S, Nayak A, Vijayakumar K, Misri Z, Suresh B, Ganesan S, Joshua AM (2011)
Comparison of physio ball and plinth trunk exercises regimens on trunk control and functional
balance in patients with acute stroke: a pilot randomized controlled trial. Clin Rehabil
25(8):709–719
16. Brock K, Haase G, Rothacher G, Cotton S (2011) Does physiotherapy based on the Bobath
concept, in conjunction with a task practice, achieve greater improvement in walking ability in
people with stroke compared to physiotherapy focused on structured task practice alone?: a
pilot randomized controlled trial. Clin Rehabil 25(10):903–912
17. Serrao M, Mari S, Conte C, Ranavolo A, Casali C, Draicchio F, Di Fabio R, Bartolo M,
Monamì S, Padua L, Pierelli F (2013) Strategies adopted by cerebellar ataxia patients to
perform U-turns. Cerebellum 12(4):460–468
Rehabilitation in Polytrauma
35
E. Spadini
Perceptive surface (SUPER) represents a new therapeutic system based on

interaction between the body surface of the patient and a perceptive support through
small latex hemispheres. Hemispheres consist of materials varying in height and
elasticity and are applied to the bed. Patient is laid up on the bed, stimulating
cutaneous and proprioceptive receptors and allowing an antalgic reflex and a
relaxing action.
35.1 SUPER in the Proprioceptive Rehabilitation

of Polytraumatized Patients
In our case series, we present four cases of high-energy fractures and internal
injuries in polytraumatized patients. Prolonged immobilization, the long wait for a
complete healing of internal injuries, and a precarious stabilization of the fractures
prevented carrying out other rehabilitative treatments.
Our sample is composed of four patients, three males and one female between 25
and 42 years old, coming into our department from the Emergency Room. All
patients had multiple fractures and internal injuries (liver, lung, spleen, kidney,
bladder).
Generally, treatment was articulated in 6 sessions of 1 h per week for a month
and then three weekly sessions of 45 min. Duration of stay in the hospital was from
45 days to 3 months.
SUPER hemispheres were composed of latex applied to a bed, positioned next to
the body surface of the patient. Hemispheres vary in height, from 4 to 8 cm, and
elasticity, being composed by materials of different characteristics that can resume
as soon as possible the original form.
E. Spadini
Neuromotor Rehabilitation Unit, “San Filippo Neri” Hospital, Rome, Italy
e-mail: e.spadini@sanfilipponeri.roma.it

352 E. Spadini
There are three types, corresponding to different colors: yellow, a soft surface;
pink, hard surfaces; and blue, harder surfaces. Altogether, hemispheres create a
perceptive support that interacts with patient’s body surface. Different degrees of
elasticity, different heights, and their location are determined by the operator.
The first session was for sensory-motor evaluation: it was to keep confidence
with the tool, using the average modulus (pink) as a reference midline and the
remaining neutral (yellow). Essential conditions for the therapeutic effectiveness
were mastoid reference alignment for anatomical median line, the comfort of
patient, the contact surface with the body surface, and the guidance of the therapist.
After a few minutes of adaptation and relaxation, the perception of the patient was
assessed qualitatively (recognition of stocks) and quantitatively. The patient was
asked to describe the sense of body position in general and then in particular the
symmetry of loading and the symmetry of the trunk; the curves of the spine; any
torsions, translations, and rotations; the support of the foot; and the presence of
minor or plus areas of support. After about 30 min, skin signs, left by hemispheres,
were evaluated.
Further processing is divided into a perception stage, a perceptual-motor stage,
and an active phase, which imply different moments and whose aims are, respec-
tively, recovery of ability to gather information from surfaces of the trunk and the
trunk capacity of fragmented elements significant for the task.
35.2 Case Description
Male patient, 42 years old, was admitted to our department for neuromotor
rehabilitation, with a diagnosis of polytrauma, left acetabular fracture, diastasis
(6 cm) of the symphysis pubis, liver laceration, large open abdominal injuries,
ablation of the spleen, and bladder trauma. The prospect of prolonged immobiliza-
tion, the long wait for a complete healing of internal injuries, a poor stabilization of
the pelvis, and a new intervention for the implementation of fixing, in which the
pieces could not be subject to the risk of a septic state, have prevented from carrying
out other rehabilitative treatment (Fig. 35.1).
SUPER rehabilitation program was carried out in daily sessions for 1 month
(1 h) and then three weekly sessions of 45 min (Fig. 35.2).
At the end of rehabilitation, we observed an acceptable realignment of bone
heads in all cases and a complete recovery of deambulation, pain reduction as
demonstrated by VAS, a good postural control with a full consciousness of the
anatomical median line and the body surface, and, finally, a good motor func-
tional outcome. SUPER showed a useful alternative treatment where we cannot
resort to other therapeutic means. More studies should be conducted to analyze
SUPER.
35 Rehabilitation in Polytrauma 353
Fig. 35.1 MS CT scan

of the described patient
Fig. 35.2 The bed

for perceptive surface
Acupuncture and Chinese Medicine:
Cervical Disorders and Chronic Pain 36
G. Garozzo
36.1 Introduction
Regarding Chinese medicine, there is always a little bit of prejudice by traditional

medical doctors and it is often proposed asthe last chance of therapy, whenever
other tretments have failed to cure.
Studying acupuncture with my great Master and Professor, Nguyen Van Ngh, I
could observe similarities between the traditional Western medicine and the Chinese
one rather than highlight differences [1].
When we talk about medicine, we speak about man, as such, but more as a part
of this universe. And it is this, or rather the laws that govern our universe, that make
the two medicines (Western and Eastern) the same. The two medicine should never
be regarded as conflicting with each other but rather agreeing on the pursuit of
health for man.
Prof. Dr. Nguyen Van Nghi has spent all his life in the quest for integration
between the two schools of medicine, and he did so through his 10-year study, being
able to match part of the famous Rosetta Stone that would allow us to translate a
language (such as the synthetic Oriental Medicine) into the analytic of our Western
culture.
This integration should not be seen reductively in an explanation of the effects of
acupuncture (considering the possible outcomes of Oriental Medicine) as the result
of a reflex system. In literature, it has been reported from many years that acupunc-
ture act at a spinal level, modulating the transmition of nociceptive information to
the central nervous system and these concepts have been written. However, stimu-
lating acupuncture points with needles, hands or anything else is not only “evoking
a reflex”, but include a more complex emotional individual response. In the same
G. Garozzo
Acupuncture and Traditional Chinese Medicine,
Artemedica via privata Angera 3, 20125 Milano, Italy
e-mail: gaudenzio62@msn.com

356 G. Garozzo
manner, smiling “after receiving a caress” or “meeting someone you love” is not
only a reflex.
Firstly, we want to focus that Traditional Chinese Medicine is one of the oldest
Schools of Medicine. The concepts with which it deals with Traditional Chinese
Medicine starts considering that man is indivisible, and that there is an intersection
between the soma and the spirit; therefore, physiological, chemical and pathological
rules are based on this concept of energy, called “qi”. Disruptions of the flow of
energy thorugh the body are believed to be responsible for disease. It is a genuinely
fascinating medicine, its diagnostic approach which takes into account the unique-
ness of Man is very advanced considering unsuspected relationships still to be
proved by western medicine.
For example, in Oriental Medicine we speak of the heart as the center of the
whole human being and as emperor (using the way they speak) of a universe
related to it. Saying so, it explains the functions and relationships, and one of them
is its ability to be the element of “fire” of the entire body (the one that heats and
burns). Well, myocardial cells produce two hormones, ANP and BNP, that are able
to stimulate lipolysis and thermogenesis, two processes known to consume fats
(ANP was discovered in 1981 by a group of experts in Kingston, Canada, led by
Adolfo J. de Bold, after noting that the injection of extracts of atrial tissue [but not
ventricular] in laboratory mice caused abundant natriuresis [release of sodium in
the urine]).
The ANP is involved in the homeostatic control of water, sodium, potassium
and fat that is present in the organism. It is released in response to an excessive
increase in blood volume (high blood pressure) by particular myocytes, in the
auricola of the right atrium of the heart. The ANP acts on the kidneys, to reduce
the water, sodium and adipose loads in the circulatory system, thereby lowering
blood pressure.
BNP (brain natriuretic peptide) is a vasoactive hormone secreted by the heart – to
be exact, by the ventricles – in response to excessive dilation or increased wall
stress.
So the two medicines speak the same language but must be analyzed by a tool
that can be the equivalent of the Rosetta Stone.
Starting from this premise, it is therefore imperative in order to understand the
explanation of pathological mechanisms, to know a bit about the organization of our
bodies according to the Eastern point of view.
From an anatomical point of view, provided with the understanding of the ana-
tomical and physiological common acquisitions, Chinese medicine tells us about
other structures of different types of energy. Briefly, we can say that in addition to
muscles, tendons, blood vessels, tissues, and others, Chinese medicine tells us about
the energetic pathways that give us the opportunity to communicate and distribute
the set of all the energies in our bodies.
These are called meridians, or as they are called in Chinese “jing luo.” In fact,
Chinese medicine does no more than clarify the effect and function of substances
such as hormones, whose qualities and functions we know, but we believe then that
they can only move through traditional anatomical pathways.
36 Acupuncture and Chinese Medicine: Cervical Disorders and Chronic Pain 357
So to exemplify all, we say that there are different locations and functions of this
pathway, enabling us to divide them as follows:
1. Main meridians or jing mai (12)
2. Secondary meridians are the following:
(a) jing jin or tendino-muscular meridians (associated in group of three and
divided into yin and yang meridians);
(b) jing bie or divergent meridians (associated in pairs respecting Internal-
External the rule, or “biao-li” in Chinese);
(c) connecting meridians at the Luo points: the 12 regular meridians, externally-
internally related in pairs, are linked together by the Luo (connecting) points e
related connenting meridians (16 for the former and 12 for the scondary in order
to correlate each yin primary meridian with its yang primary meridian); and
(d) qi jing ba mai or 8 extraordinary vessel (in number of eight associated in
pairs).
The different energies can instead be divided into several groups, but for the sake
of simplicity, just remember:
(a) Ying Qi – also called Nutritive Energy
(b) Wei Qi – also called Defense Energy
(c) Jing Qi – also called Acquired Energy
(d) Shen Qi – also known as Mental Energy
(e) Yuan Qi – also called Ancestral Energy
(f) Tian Qi – also called Respiratory Energy
(g) Gu Qi – also called Food Energy
(h) Zong Qi – also called Pectoral Energy
36.2 The Tendon-Muscular Meridians (TMM)
The TMM are large vessels that:

1. Start from jing distal points
2. Affect the tendons and muscles
3. Do not penetrate the organs and viscera,
4. Their paths go from bottom to top
5. Play a significant role in the disease known as “external factor”
6. Are not subject to the laws of Yin/Yang alternation.
The three yang meridians of the foot correspond to spring, which are the first,
second and third months of the lunar year:
• TMM Stomach is the first month
• TMM Bladder is the second month
• TMM Gall bladder is the third month.
The three yin meridians of the foot correspond to autumn, i.e., on the seventh,
eighth and ninth months of the lunar year:
• TMM Spleen/Pancreas is the seventh month
• TMM Kidney is the eighth month
• TMM Liver is the ninth month
358 G. Garozzo
The three yang meridians of the hand correspond to summer, i.e., the fourth, fifth
and sixth months of the lunar year:
• TMM Intestine is the fourth month
• TMM Small intestine is the spring month.
• TMM San Jiao (also commonly and incorrectly called Triple Burner) is the sixth month
The three yin meridians of the hand correspond to winter, i.e., the tenth, eleventh
and twelfth months of the lunar year:
• TMM Pericardium is the tenth month
• TMM Lung is the eleventh month
• TMM Heart is the twelfth month
36.2.1 Bladder
Disorders of the TMM of the bladder (Fig. 36.1) are popliteal muscle contractures,
the feeling of a broken spine, contracture of the tendons and muscles of the neck,
inability to raise the arm, stabbing pain in the axilla and the supraclavicular fossa,
headache, and facial neuralgia.
Fig. 36.1 Start at the

external corner of the nail of
the 5th finger (B67) up to the
lateral aspect of the knee
(B39), from here: a vessel
goes down to the heel, back
to the popliteal fossa (B40); a
vessel up to the buttock, the
medial part of the back and
reaches the neck (B10),
reaches the base of the
tongue, a vessel reaches the
skull down to the m around
the eye (B2), cheekbone; a
vessel reaches the armpit,
St12 and reaches the mastoid
Fig. 36.2 Starts at the external nail

of the 4th toe (GB44), climbs the
outside face of the legs, inserted on
the knee, penetrates to the area of
“rabbit crouching” (St32), reaches
the thigh and the hip, where a
vessel surrounds the buttock, and
arrives at the coccyx (DU1). The
main vessel climbs to the false ribs,
divides into two branches, one
arriving at the breast to the
supraclavicular fossa St12, the other
goes to St8, rises to Baihui, comes
back down to the chin and
cheekbone SI18, and enters the
bone in the external commissure of
the eye
32E
36.2.2 Gall Bladder
Disorders of the TMM of the gall bladder (Fig. 36.2) are the inability to stretch and
flex the knee associated with pain in the popliteal fossa, pain in the antero-external
part of the thigh to the hip, pains in the side up to the ribs, side, chest, breast, supra-
clavicular region, contracture and pain in the leg up to the lateral malleolus, and
contracture of the 4th toe.
360 G. Garozzo
Fig. 36.3 Starts from the

external side of the nail of the
2nd, 3rd and 4th toe, rises to
the instep and is divided into
two branches. The external
branch goes up to the Huan
Tiao hip point (GB30), goes
to the false ribs and is
inserted on the spine (DU9).
The internal branch goes
from the dorsum of the foot,
climbs to below the patella
and joins the regular meridian
of GB; The vertical section
runs through the area of the
“rabbit crouching” (St32),
arrives at Scarpa’s triangle,
up to RM2 and goes to the m.
rectus abdominis, rising up to
St12 to the cheekbone (SI18)
and to the nose, then to the
regular meridian of bladder
36.2.3 Stomach
Disturbances of TMM of the stomach (Fig. 36.3) are swelling below the groin,
orchitis, contracture and stiffening of the dorsum of the foot, contracture of the
thigh area known as “rabbit crouching,” contracture and tightening of the abdominal
muscles, sudden deformation of the mouth, pain radiating to the supraclavicular
fossa and cheek, contracture of the 2nd toe and leg.
36.2.4 Spleen/Pancreas
Disturbances of TMM of the spleen (Fig. 36.4) are pain in the tibia and knee, pain
in the medial side of the thigh, up to the groin, shooting pains in the external
Fig. 36.4 Starts at the

medial corner nail of the big
toe, goes to the internal
malleolus, ascends along the
medial aspect of the thigh,
reaches Scarpa’s triangle,
converges towards the
external genitalia, penetrates
the abdomen, reaches the
navel, and then the ribs and
the internal part of the thorax.
A vessel, from the external
genitalia, arrives at the spine
genitals, pain in the navel and hips, widespread pain in the chest and spine,
contractures and cramps in the big toe and the internal malleolus.
36.2.5 Liver
Disturbances of TMM of the liver (Fig. 36.5) are contractures and pain in the
medial thigh muscle, pain to the tibia tuberosity and medial side of the knee, pain
in the big toe up to the internal malleolus, and genital disorders with
impotence.
362 G. Garozzo
Fig. 36.5 Starts at the big toe, climbs in front of the

internal malleolus, passes forward to the spleen jing jin,
following the tibia right below the internal tuberosity, up to
the groin, converges to the external genitalia to get together
with other MTM in the suprapubic region to RM3
36.2.6 Kidneys
Disturbances of TMM of the kidney (Fig. 36.6) are contractures and pain along the
entire path, contractures of the plantar muscles, abdominal contracture with the
sensation of an anterior weight on the body associated with limiting the ability to
bend backwards, abdominal contracture to the external side with a sensation of
weight lumbar associated with a limitation to bend forward.
Fig. 36.6 Starts below the 5th

toe, reaches Ki1 and follows the
TMM of the spleen up to the
internal malleolus. Reaches the
heel, ascends along the medial
aspect of the leg to the internal
tuberosity of the tibia, then up to
the groin. Converges in the
genital region, penetrates the
abdomen (RM3) and following
the anterior aspect of the spine, a
vessel starts to the genital area,
passes through the buttock of the
opposite side, follows the lateral
aspect of the spine, up to the
occiput and joins with the TMM
of the bladder to B10
36.2.7 Small Intestine
Disturbances of TMM of the small intestine (Fig. 36.7) are pains in the back side of
the shoulder to the neck, hearing loss, pains in the ear and chin, eyes closing a
moment before looking, muscular contracture of the neck (torticollis), possible pain
throughout the path of TMM, internal side pain of the arm from the armpit to the
little finger.
364 G. Garozzo
Fig. 36.7 Starts at the external

side of the little toenail, goes to
the medial epicondyle, reaches
the armpit, goes around it,
goes to the back side of the
shoulder, then up to the neck
where it divides into two
branches: the secondary branch
goes to the mastoid, goes
around the ear, then to the jaw
and up to the outer canthus of
the eye. The main branch goes
on the corner of the jaw, St6,
passes in front of the tragus, up
to the outer corner of the eye
and ends at the fronto-parietal
region
36.2.8 San Jiao
Disturbances of TMM of san jiao (Fig. 36.8) are contracture and cramping of the
entire path, contracture and retraction of the tongue.
Fig. 36.8 Starts at the external corner of the nail of the 4th
finger, goes to the wrist, follows the medial part of the forearm,
inserted the olecranon, and climbs up to the shoulder and neck,
joins the regular meridian, arrives at the corner jaw (SI17) and is
divided into two branches: a vessel enters the throat, reaches the
base of the tongue; a vessel from the corner jaw goes to St6,
passes in front of the ear, comes to the outer corner of the eye, and
fits on the front of the St8
36.2.9 Large Intestine
Disturbances of the TMM large intestine (Fig. 36.9) are “helmet headache,” inability
to raise the arm, inability to turn the neck, pain, contracture and cramping on the path.
366 G. Garozzo
Fig. 36.9 It starts at the external corner of the index fingenr’s nail, climbs along the outer edge of
the arm (LI11), reaches the jianyu point (LI15) on the shoulder and is split: a branch goes around
the shoulder and goes to DU14.The main branch rises to St6, and is divided into two branches, one
in the jaw and the other in the cheekbone, one on the forehead at PC 9 up to the corner jaw on the
opposite side
36.2.10 Lung
Disturbances of TMM of the lung (Fig. 36.10) are a sore shoulder that cannot be
lifted, hypocondralgia, and sometimes haematemesis. The pain, very sharp, causes
anxiety and oppression. The muscles on the course of the meridian are contracted
or sore.
Fig. 36.10 Starts at the inner

corner of the thumb nail, goes
up to the thenar eminence,
passes the external side of the
wrist (L10), follows the forearm
up to the center of the elbow,
back along the medial surface of
the arm, enters the armpit, goes
to GB22, reappears in the
supraclavicular fossa at St12,
penetrates into the chest until
the it reaches the cardias, goes
deeper into the thorax up to the
cardias, then reaches the ribs up
to RM17 and then to the
diaphragm and the cardias
36.2.11 Xin Bao
Disturbances of TMM of xin bao (Fig. 36.11) are chest pain, axillary pain,
oppression, contracture and pain on the course of the meridian.
36.2.12 Heart
Disturbances of the TMM of the heart (Fig. 36.12) are the clogging syndrome of the
energy at the navel, contractures and pain with a sense of snare at the elbow,
contractures and pain in the chest with a painful contracture along the path.
368 G. Garozzo
Fig. 36.11 Starts on the external

corner of the nail of the middle
finger, reaches the center of the
elbow, follows the medial side of
the arm, fits under the armpit and
branches to the ribs. A vessel
penetrates deep into the arm,
arrives at the inner part of the
chest and goes into the cardias
36.3 Whiplash-Associated Chronic Pain Treatment
Acupuncture is widely used for the treatment of neck and other musculoskeletal
pain, and there is some evidence supporting its effectiveness for short-term pain
relief. The effectiveness of acupuncture in the treatment of whiplash-associated dis-
orders is not clear and, in my experience, the Quebec classification (orthopedic
relevance, racture or dislocation of the vertebrae or intervertebral discs with spinal
cord compression) and the outcome of whiplash to surgical procedure has to be
considered in any way. Considering the classification of the Quebec Task Force,
whiplash grade 0-1-2 can be combined and treated as a syndrome of TMM, while
grade 3 is related to the Longitudinal Luo of Du Mai Syndrome, although symptoms
may persist and then we can find a simultaneous involvement of TMM. We will not
Fig. 36.12 Starts at the internal

side of the little fingernail, goes to
the styloid process of the ulna, up
to the medial aspect of the forearm
to the elbow, reaches the armpit
and joins with TMM of the lung
and SJ to 22GB. Penetrates into
the chest and continues into the
interior space of the breast, goes to
RM17 and down to the cardias and
then reaches the navel
consider level 4 in any way because it has to be dealt with in the vascular/orthope-
dics/surgical field.
When there are symptoms resulting from whiplash, we will certainly find the
symptoms that usually accompany you when the tendino-muscular meridian (TMM)
and the Luo of Du Mai are involved [2] – not only the path, but above all the special
form of presentation (traumatic and therefore recently acquired) that characterize
the pathology of this particular type of energies‘ pathways. That said, it is also nec-
essary to make clear that if the treatment is not for a recent whiplash injury, but for
a chronic form of symptoms, it may no longer reflect the pathology of these types
of energetic pathways but would cover other types of them, which would better
explain the chronic painful traumatic event [3].
370 G. Garozzo
Many patients with whiplash-associated chronic pain show features of central

sensitization. Randomized trials examining whether treatments are able to influence
the process of central sensitization in patients with chronic WAD are emerging.
Acupuncture results in activation of endogenous analgesia and relief in symptoms
in patients with chronic WAD Quebec 1-2-3.
Tobbackx et al. [4], through a randomized crossover pilot trial with blind asses-
sors, that was performed on 39 patients, have recently shown that local baseline
pressure pain sensitivity and during conditioned pain modulation decreased more
significantly following acupuncture compared with simple aspecific relaxation, both
in the neck and at a site distinct from the painful region. When comparing the long-
term effects of acupuncture versus relaxation, no differences were observed in con-
ditioned pain modulation, temporal summation of pressure pain, neck disability, or
symptom severity. Their findings suggest that acupuncture treatment activates
endogenous analgesia in patients with chronic WAD at least in the short-medium
period [5].
The ancient texts of Nei Jing: Ling Shu, and Su Wen describe the treatment to be
carried out according to the pathological state of the event, considering first of all
the interest of the surfaces:
• Disease found in the skin: insert the needle into the distal jing points of the
meridians Interested, jing jin. Treatment of jing distal point, toning point of the
meridian, ashi point in dispersion; for the treatment of TMM.
• Disease is in the subcutaneous tissue: insert the needle into the Luo and Shu
points of the meridians involved. For the treatment of Luo M.
• Disease is in deep tissues (muscles, bones and joints, after passing the surface
layers and the subcutaneous): insert the needle into the Jing proximal points of
the yin meridians and the He points of yang meridians. For the treatment of rheu-
matic disorders.
• Disease (humidity) is in the yin meridians of the lower: o needle the distal jing points
and the ying points. For the treatment of rheumatic syndromes located at the bottom.
36.4 Clinical Practice
36.4.1 TMM
Observe whether the radiation of pain extends along the path of TMM.
Check if the point of union of the 3 TMM involved is painful on palpation.
Check the organ/bowels of the main meridian involved.
36.4.1.1 Needling – Declaration of Qi Bo

Needle the distal point jing.
Tonify the main meridian.
Puncture with a needle the point where the three TMM
Puncture with a needle the painful points (ashi) in dispersion, then continue
using the stimulator.
Example 1:
Facial pain – TMM yang of the foot (meeting point SI18)
If the pain goes down to the lower jaw moving from the temporal area:
facial point + tones the regular meridian of the gall bladder.
If the pain is associated with the inner corner of the eye: facial point +
tones the regular meridian of the urinary bladder. If pains go to the wing of the
nose, lips, inner corner of the eye: facial point + tones the regular meridian of
the stomach.
(Points to tonify: GB43, B67, ST41; Shu points: GB41, B65, ST43.)
Example 2:
Migraine – TMM yang of the hand (meeting point St8-GB13)
If the pain goes to the outer corner of the eye, ear, jaw, neck, shoulder:
painful point + tonify the regular meridian of the small intestine.
If the pain goes to the outside corner of the eye, neck, shoulder, and throat,
with a contraction of the tongue: painful point + tonify the regular meridian of
San Jiao.
If the pain goes to the cheekbone, if you feel the sensation of a helmet that
surrounds the forehead and goes to the opposite side of the jaw: painful point
+ tones the regular meridian of the large intestine (Points to tonify: SJ3, SI3,
LI11; Shu: SJ3, SI3, LI3).
Example 3:
Subaxillary pain – TMM yin of the hand (meeting point GB22)
Pain accompanied by a small pain in the shoulder, chest: painful point +
tonify the regular meridian of lung.
If it is accompanied by oppression with pain in the hips and chest: painful
point + tonify the regular meridian of Xin Bao. If it is accompanied by pain
between the heart and navel: painful point + tonify the regular meridian of the
heart: subaxillary pain.
(Points to tonify: PC9, Ht9, L9 Shu; PC7, HT7, L9)
36.4.2 Luo Vessel of Dumai-DU
This vessel starts from Changqiang (DU 1) located at the end of the coccyx and goes
up to the heart where it branches toward the shoulder.
It communicates with the bladder meridian at the B10 point and penetrates
deeply into the muscles. Symptoms may be divided into symptoms of fullness
372 G. Garozzo
(stiffness of the spine) or symptoms of feeling empty (dizziness with a heavy

head).
In the case of “fullness,” the treatment is to disperse Changquiang (DU1), while
in the case of the “empty feeling,” it is necessary to tonify Changquiang (DU1).
Conclusions
Acupuncture is a well-tolerated treatment for people with chronic WAD pain.
The main effects are more evident in the short and medium run, thus it is useful
to combine Chinese medicine techniques with the traditional western medicine
therapies. Findings suggest that acupuncture treatment activates endogenous
analgesia in patients with chronic WAD, that acupuncture is more effective than
no treatment, a sham, or alternative [6–8] interventions but also that it is often
necessary to combine it with manual and supervised exercise interventions and
low-level laser therapy.
For whiplash-associated chronic pain, without radicular symptoms, interven-
tions that focused on regaining function as soon as possible are relatively more
effective than interventions that do not have such a focus.
References
1. Nguyen-Van-Nghi, Fisch G, Kao J (1973) An introduction to classical acupuncture. Am J Chin
Med (Garden City NY) 1(1):75–83
2. Rosted P, Jørgensen A (2009) Acupuncture for a patient with whiplash-type injury. Acupunct
Med 28(4):205–206
3. Chen Y, Zheng X, Li H, Zhang Q, Wang T (2011) Effective acupuncture practice through
diagnosis based on distribution of meridian pathways & related syndromes. Acupunct
Electrother Res 36(1–2):1–18
4. Tobbackx Y, Meeus M, Wauters L, De Vilder P, Roose J, Verhaeghe T, Nijs J (2013) Does
acupuncture activate endogenous analgesia in chronic whiplash-associated disorders? A
randomized crossover trial. Eur J Pain 17(2):279–289
5. Cameron ID, Wang E, Sindhusake D (2011) A randomized trial comparing acupuncture and
simulated acupuncture for subacute and chronic whiplash. Spine (Phila Pa 1976) 36(26):E1659–
65. doi: 10.1097/BRS.0b013e31821bf674
6. Hurwitz EL, Carragee EJ, van der Velde G, Carroll LJ, Nordin M, Guzman J, Peloso PM,
Holm LW, Côté P, Hogg-Johnson S, Cassidy JD, Haldeman S, Bone and Joint Decade 2000–
2010 Task Force on Neck Pain and Its Associated Disorders (2008) Treatment of neck pain:
noninvasive interventions: results of the Bone and Joint Decade 2000–2010 Task Force on
Neck Pain and Its Associated Disorders. Spine (Phila PA 1976) 33(4 Suppl):S123–S152
7. Hurwitz EL, Carragee EJ, van der Velde G, Carroll LJ, Nordin M, Guzman J, Peloso PM,
Holm LW, Côté P, Hogg-Johnson S, Cassidy JD, Haldeman S (2009) Treatment of neck pain:
noninvasive interventions: results of the Bone and Joint Decade 2000-2010 Task Force on Neck
Pain and Its Associated Disorders. J Manipulative Physiol Ther 32(2 Suppl):S141–S175
8. Bismil Q, Bismil M (2012) Myofascial-entheseal dysfunction in chronic whiplash injury: an
observational study. JRSM Short Rep 3(8):57
Acupuncture and Chinese Medicine:
Equilibrium Disorders 37
P.L. Ghilardi, C. Borsari, A. Casani, L. Bonuccelli,
and B. Fattori
37.1 Introduction
Acupuncture [1] may be considered a valid and efficacious tool in the treatment of
cervically originated vertigo, since it intervenes on a known physiopathological
substrate [2]. It exerts its function through the activation of the transducers in the
skin and in the surface and deep muscles in the neck, which are capable of affecting
the vestibulospinal reflex arc [3, 4].
It is well known, in fact, that vestibulospinal reflexes play a fundamentally
important role in the maintenance of posture [5].
The above-mentioned physiopathological considerations prompted us to apply
acupuncture (particularly as reflex therapy) to disorders in which there is a preva-
lent alteration in the macular and cervical inputs; this is seen at its utmost in
trauma from cervical torsion. In fact, in these patients particularly there is an alter-
ation in the cervical proprioceptive inputs due to stretching of the neuromuscular
spindles and the osteo-tendon articulation receptors in the neck [6]. In patients
affected by balance disorders of cervical origin and particularly in those with
whiplash injury (WI), there is a prevalence of postural disorders linked with alter-
ations in the VSR (vestibulospinal reflex) over those related to VOR (vestibu-
loocular reflex). For this reason, posturographic examination appears to be the
most appropriate method for both qualitative and quantitative clinical assessments
of the alterations in the postural patterns of these patients and for monitoring their
follow-up [7, 8].
P.L. Ghilardi • A. Casani • L. Bonuccelli • B. Fattori (*)

Institute of Otorhinolaryngology, University of Pisa, Pisa, Italy
e-mail: bfattori@ent.med.unipi.it
C. Borsari
3rd Department of Anesthesiology, Santa Chiara Hospital, Pisa, Italy

37.2 Methods
Posturographic examination is performed first of all in OE conditions (open eyes)

with the patients gazing at an illuminated spot, then in CE (closed eyes). In this
routine posture test, we also used sensitisation tests to eliminate and/or disturb one
or two of the three sensitive entrances to the posture system (visual, proprio-
exteroceptive and vestibular). Two of these tests which we routinely applied were
the head retroflexion test (CER) and the head shaking posturography test (CE HST).
The posturographic examination of the patient was performed, during the first ses-
sion, with three investigations consisting each of four tests: OE, CE, CER and
CEHST. The first investigation was performed in basal conditions. The second was
carried out after simulating acupuncture, that is, by placing four needles on random
points of the cervical region so that the patient could feel only subjective
stimulation.
This simulation of acupuncture before the true acupuncture session served to
exclude the presence of functional components. The third investigation was per-
formed immediately after the actual acupuncture. Thereafter, further sessions were
carried out once a week for 3–5 weeks according to the patient’s clinical response,
and they were always monitored with posturography.
We evaluated by computerised static posturography the postural changes after
acupuncture treatment in a group of 27 patients (12 men and 15 women; mean age,
35.7±6.8 SD) having balance disorders caused by cervical torsion due to whiplash
injury [9].
Acupuncture was performed by piercing deeply and bilateral1y points 10 V
(Tienn Chou) and 20VB (Fong Tcheou) with steel needles which were twirled
manual1y for 20 s after insertion. Each session lasted 20 min. We chose these acu-
puncture points on the basis of the long-established Chinese experience in this field
[10, 11].
However, other points may be used with equal results (17TR, 3IG, 62V, ear
points, scalp puncture, etc.), though we have not used them in order to maintain
uniformity in the investigation. The posturographic examination in our patients
with WI confirmed alterations in both OE and CE in 45 % of the cases, though no
specific pattern could be distinguished.
The control group consisted of 25 patients complaining of the same symptoms as
those recorded by the study group due to whiplash injury but treated with nonsteroi-
dal anti-inflammatory drugs and myorelaxation or with physiotherapy only.
The stabilogram gave a prevalence of wide and arrhythmic oscillations on both
planes, though the sagittal plane prevailed over the other (Fig. 37.1). The statoki-
netic parameters showed an increase, particularly, in the surface. The centre of grav-
ity often appeared shifted to one side (Fig. 37.2).
These findings were seen to be altered even more in the sensitisation tests, par-
ticularly, when the head was retroflexed (Fig. 37.3). In CE and CER, analysis peak
on 0.1–0.2 Hz of the Fourier spectrogram revealed frequencies shifted towards
0.1–0.2 Hz (Fig. 37.4).
After the first acupuncture session in our experiment, we noticed an improve-
ment in stance in 75 % of our patients. Nevertheless, this result was transient in the
majority of cases; once the acupuncture sessions were repeated, this improvement
tended to stabilise. After the three to five sessions of acupuncture on our group of
37 Acupuncture and Chinese Medicine: Equilibrium Disorders 375
(mm)
Stabilograms
5.7
D
3.4
1.1
x mean:
2.0 mm
−1.1
–
2s
−3.4
S
−5.7
(mm)
5.7
A 3.4
1.1
Y mean:
−33.6 mm
−1.1
−3.4
I
−5.7
–
2s
Fig. 37.1 Stabilograms: prevalence of wide and arrhythmic oscillations on both planes, with
prevalence on sagittal plane
Statokinesigram
Fig. 37.2 Statokinesigram:

the centre of gravity appears
shifted to the left –2.0 cm. –3.0 cm.
Fig. 37.3 Test performed in

100
CE: the Fourier spectrogram
shows a maximal frequency FFT in X
80
fmax=
60 .11719
40
20
.02 .1 .5 1 2.5 5
100
FFT in Y
80
fmax=
.13672
60
40
20
.02 .1 .5 1 2.5 5
Statokinesigram
–2.0 cm. –4.9 cm.
Fig. 37.4 CER test: the statokinesigram shows a remarkable increase of surface
patients with cervical torsion trauma, 60–70 % of the balance disorders were cured,
whereas 20 % showed considerable improvement as compared with the initial con-
ditions. The results were nonsatisfactory in only 10–20 % of the patients, either
because of a lack of response to acupuncture treatment or due to rapid regression of
the improvement achieved once the sessions were over. Cervical torsion trauma and
balance disorders with cervical origin in general, such as those connected with pro-
nounced antalgic contracture of the nape muscles due to cervical arthrosis, are the
conditions which responded best to acupuncture. In fact, other groups of patients
suffering from vertigo of other natures did not respond so well.
In central-type disorders (vasculopathies or neurodegeneration), we saw no posi-
tive response to acupuncture in any of the patients we treated and who were always
submitted to posturography in the same manner as described before. In the cases of
monolateral peripheral vestibular deficiency, we encountered positive responses to
acupuncture in 35 %, while no statistically significant improvement (p > 0.1) was
seen in the posturography performed n the group of patients with cupulolithiasis.
Conclusions
Posture study with the aid of a stabilometric platform can supply an objective
assessment of acupuncture efficacy, particularly, in patients with balance disor-
ders of cervical origin. In fact, the stabilometric examination permits quantifying
the various postural parametres and gives a graphic description of any shifting in
pressure centres on both sagittal and transversal planes; hence it is possible to
perform a series of repeated tests which are perfect1y comparable with each
other. The patients suffering from central-type vertigo disorders, mainly vascu-
lar, showed very few variations in stance both before and after acupuncture. The
most interesting results were accomplished in the group of patients with balance
disorders of cervical origin; these cases showed satisfactory results right from
the first acupuncture session, and the postural parametres of the four stabilomet-
ric tests became normal in 75 % of the cases. Even the patients with peripheral
vestibular disorders, particularly monolateral vestibular damage, had interesting
results with an improvement in posture performance in 35 % of the cases, which
can very likely be attributed to a plastic and self-corrective rebuilding of the
vestibulospinal reflex (VSR) arc produced by acupuncture. Acupuncture stimu-
lation in these situations appears to activate the ascending reticulospinal cerebel-
lar pathways and, therefore, the descending projections which, from the cortical
vermis are of the basis of the VSR. There are many clinical reports which con-
firm the efficacy of acupuncture in balance disorders when performed according
to the traditional methods established by ancient Chinese energetic medicine, but
there are very few experimental data referring to the neurophysiological and/or
neuroendocrinological mechanisms of action of acupuncture in vertigo of cervi-
cal origin. In recent years much progress has been accomplished regarding the
anatomy and physiology of the acupuncture points, but, above all, modern acu-
puncture specialists have shifted their interest towards research into the physio-
logical aspects of the points. Present-day research is still far from a thorough
explanation of acupuncture, and many hypotheses have been pronounced on this
matter: the mechanisms of action are quite definitely many. Acupuncture is cer-
tainly capable of interfering with the mechanism of action of numerous neu-
rotransmitters (endogenous opioids, serotonin, P substance, catecholamine,
GABA, cortisol, etc.), and it also provokes excitation reflexes and inhibition of
the spinal cord (grey gel substance of the periaqueduct), of the bulbar areas
(reticular substance) and of the thalamic and cortical regions. Another possible
mechanism of action which must be considered, especially in cases of vertigo of
cervical origin, is a sympathicolytic action exerted via inhibition of the brain-
stem reticular substance. These data indicate that this treatment is capable of
direct1y modifying the reflexes which start from the cervical region and which
are responsible for balance disorders. One must also take into account an antie-
dema activity, however, which can reduce the effects of pressure on the posterior
roots of the cervical nerves and also a more generalised activity of stabilisation
of the basilar vertebral system. The positive effects manifest immediately after
even just one acupuncture session; nevertheless, in this experiment, we noticed a
decrease in efficacy during the following days which required a series of further
sessions of acupuncture in order to stabilise the results, as seen in the follow-up
of these patients. The high percentage of positive responses, particularly in the
cases of vertigo of cervical origin and less so in those with monolateral periph-
eral vestibular deficiency, leads us to advocate the therapeutic efficacy of acu-
puncture, at least in disorders in which it can be associated with or proven as a
valid alternative to pharmacological treatment.
No statistically significant advantage of the acupuncture (or laser acupunc-
ture) treatment was found [12] in the acute phase regarding mobility in all three
planes, duration of pain and duration of use of a cervical collar, that to say prob-
lems regarding myofascial pain and headaches while, in our experience, in the
chronic phase of whiplash associated vertigo and dizziness, a considerable
reduction of the postural sway that can be obtained. In fact the frequency oscil-
lation on the sagittal plane in CER was reduced in the study group, whereas we
noticed a progressive increase of its values in the control group. The high per-
centage of positive results in whiplash injury patients leads us to advocate
acupuncture for chronic balance disorders due to whiplash.
References
1. Chen Zheng Qiu (1993) Participation of GABA in sn emanating descending modulation on the
nucleus centrum medianum in motor cortex in acupuncture analgesia. Word J Acupunct
Moxibust 3:46–50
2. Coan RM, Wong G, Coan PL (1982) The acupuncture treatment of neck pain: a randomized
controlled study. Am J Clin Med 9:327–332
inputs on vestibulospinal neurons. J Neurophysiol 45:852–868
4. Han J (1988) Central neurotransmitters and acupuncture analgesia. In: Pomeranz B, Stux G
(eds) Scientific bases of acupuncture. Springer, Berlin/Heidelberg/New York, pp 7–33, 195
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Part V
Conclusive Remarks
Management and Treatment of WAD
Patients: Conclusive Remarks 38
D.C. Alpini, G. Brugnoni, and A. Cesarani
38.1 Introduction
Whiplash-Associated Disorder (WAD) represents a significant public health

problem, resulting in a substantial socioeconomic burden throughout the
industrialised world, wherever costs are documented.
WAD is caused by an acceleration-deceleration mechanism of energy transfer to
the neck, mainly, and the spine, generally. The most common cause of WAD is a
motor vehicle collision (MVC), but sporting accidents or falls can also cause
whiplash.
Under the point view of time course, whiplash may be classified as acute (less
than 2 weeks), subacute (2–12 weeks) or chronic (longer than 12 weeks).
Under the point of view of lesion, WAD has been classified in 1995, by the
Quebec Task Force (QTF) [1], in four progressive grades. According to the QTF,
‘whiplash is an acceleration deceleration mechanism of energy transfer to the neck,
which…may result in bony or soft tissue injuries (whiplash injury), which in turn
may lead to a variety of clinical manifestations (whiplash-associated disorders,
“WAD”)’ (Table 38.1).
D.C. Alpini (*)

G. Brugnoni
Italian Academy of Manual Medicine, Italian Institute for Auxology, Milan, Italy
A. Cesarani
Milan, Italy
Milan, Italy

Table 38.1 Quebec Task Force Classification of Grades of WAD
Grade Classification
0 No complaint about the neck
No physical signs
1 Neck complaint of pain, stiffness or tenderness only
No physical signs
2 Neck complaint and musculoskeletal signs
Musculoskeletal signs include decreased range of motion and point tenderness
3 Neck complaint and neurological signs
Neurological signs include decreased or absent tendon reflexes, weakness and
sensory deficit (e.g. hearing loss)
Neck complaint and fracture or dislocation
Many treatments have been advocated for patients with WAD, and many diagnostic
procedures have been proposed to document lesions or dysfunctions induced by whiplash,
but the majority of therapeutic interventions used in the treatment of WAD had undergone
little to no scientific investigation. Due to the paucity of scientifically rigorous studies, the
QTF was forced to rely on consensus opinion for the majority of their mandated treatment
recommendations, offering little in the way of evidence-based clinical guidelines.
The conclusive considerations and remarks presented into this chapters on one
hand are based on the main reviews [2–9] and the published guidelines [9] and on the
other hand on the personal experience in the field of diagnosis and treatment of WAD.
Under the point of view of symptoms, main WADs regard pain, especially but
not uniquely neck pain, and unsteadiness. Thus, both management and treatment in
this chapter will be focused on pain and vertigo/unsteadiness.
Management refers to the overall approach to care, or plan, formulated for indi-
vidual patients; treatment refers to the therapeutic modalities utilised as part of the
management approach, including advice and education, exercise, joint mobilisa-
tion, pharmacotherapy, etc.
38.2 Management
38.2.1 Acute and Subacute Phases
Neck symptoms, pain and stiffness, are the most common symptoms after a whip-
lash trauma. Pain often occurs soon, while stiffness can occur later.
38 Management and Treatment of WAD Patients: Conclusive Remarks 385
Thus, a comprehensive assessment and physical examination of the patient is

mandatory (see Chaps. 14 and 21).
The first aim of the assessment in the acute phase is a correct classification of the
patient in the QTF WAD grade.
Neck symptoms may exist without objective findings during clinical examination
(QTF WAD grade I). Tenderness at palpation over muscle attachments and over
muscles in the cervical spine, the shoulder region and/or the back is common (QTF
WAD grade II). Approximately 50–60 % of patients who present to emergency
rooms have QTF WAD grade II.
It is very important to take in mind that prompt and adequate management of the
acute pain reduces the risk of chronic pain.
History taking is a cornerstone of early management of WAD patients of all
grades.
Personal and circumstances of the injury have to be carefully collected [10].
Radiological procedure is preferably based on Canadian C-spine rule [11, 12]
(Table 38.2).
The most important element of initial assessment is the identification of
patients who are at risk of developing serious consequences such as fractures,
dislocations (QTF WAD grade IV) or significant neurological damage (QTF WAD
grade III).
In QTF WAD grade III, specialised imaging techniques (CT scan and/or MRI)
have to be used when nerve root compression or spinal cord injury are
suspected.
QTF WAD grade III may be estimated to be documented in 2–6 % of patients
even if 20 % of patients report neurological symptoms like paraesthesia, sensory
deficit and weakness in an arm or hand.
Dizziness and unsteadiness are very common, while true vertigo is rare. However,
when a patient complains vertigo that appears on moving the head or in postural
changes, a paroxysmal positioning vertigo (PPV) has to be suspected and adequately
treated (see Chaps. 14 and 23-I).
Tinnitus is common enough, while hearing loss is rare. However, when a patient
complains of unilateral constant and continuous tinnitus and/or unilateral hypoacu-
sia, a sensorineural sudden hearing loss (SSHL) has to be suspected and adequately
investigated and treated (see Chaps. 11, 13, and 17).
In QTF WAD grade IV, when imaging confirms the existence of a fracture, the
patient has to be immediately referred for a specialised management.
Table 38.2 Canadian C-Spine Rule
The Canadian C spine rule

For alert (GCS score = 15) and stable trauma patients when cervical spine injury is a concern
1. Any high-risk factor that mandates

radiography?
Age ≥ 65 years Yes
or Dangerous mechanism*
or Paresthesias in extremities
No
2. Any low-risk factor that allows safe

assessment of range of motion ?
a
Simple rear-end MVA
or Sitting position in Emergency No Radiography
Department
or Ambulatory at any time
or Delayed onset neck painb
* Dangerous mechanism
or Absence of midline cervical spine • Fall from elevation
tenderness >3 ft/5 stairs
Yes • Axial load to head eg, diving
• MVA high speed (>100km/h),
3. Able to actively rotate neck? rollover, ejection
45 degrees left and right Unable • Bicycle crash
a
Able Simple rear-end MVA excludes:
• Pushed into oncoming traffic
• Hit by bus/large truck
No radiography • Rollover
• Hit by high-speed vehicle
b
Delayed
• ie, not immediate onset of
neck pain
Pain intensity and disability may be quantified using the Visual Analogue
Scale (VAS) and the Neck Disability Index [13] (NDI) respectively (Table 38.3).
Table 38.3 Neck Disability Index

Table 38.3 (Continued)
Poor prognosis is associated with a high pain score (VAS > 7/10) and/or high
disability score (NDI > 40/100). The presence of either of these factors should alert
to the potential need for more regular review of treatment or earlier referral to a
specific specialist. Identification of poor prognosis patients is mandatory in order to
provide adequate prevention of chronicisation.
Reassessment has to be planned at 7 days, 3 weeks, 6 weeks and 3 months for

acute WAD.
At 3 months resolution has occurred in approximately 50 % of acute cases.
Treatment should have ceased or, if the patient is still improving, self-management
should be promoted.
Patients who still require treatment after 3 months are considered to have chronic WAD.
It could be useful to ‘measure’ the impact of WAD on patient health and life-
style through the ‘Core Whiplash Outcome Measure’ [14] (Table 38.4), a five-item
scale that is brief and user-friendly for clinicians. It measures several constructs of
health including pain, function and well-being. In addition, it measures the days
off work.
Table 38.4 Core Whiplash Outcome Measure

Persistent or recurrent vertigo and/or persistent dizziness and unsteadiness have

to be investigated.
Vestibular evoked potentials (see Chap. 17-II) are specific to detect vestibular
lesion causing relapsing positioning vertigo. Posturography allows a precise docu-
mentation of stance control disturbances (see Chap. 15); Smooth Pursuit Neck
Torsion Test (SPNTT) and Cranio-Corpo-Graphy (CCG) (see Chap. 16) allow accu-
rate documentation of cervico-cephalic dynamic control disturbances either as ocu-
lomotor (SPNTT) and gait (CCG) disturbances.
Handicap induced by persistent dizziness may be quantified by means of the
Dizziness Handicap Inventory [15, 16] (Table 38.5).
Table 38.5 Dizziness Handicap Inventory
Instructions: The purpose of this scale is to identify difficulties that you may be experienc-
ing because of your dizziness or unsteadiness. Please answer ‘yes’, ‘no’ or ‘sometimes’ to
each question. Answer each question as it pertains to your dizziness or unsteadiness prob-
lem only.
Does looking up increase your problem?
Because of your problem, do you feel frustrated?
Because of your problem, do you restrict your travel for business or recreation?
Does walking down the aisle of a supermarket increase your problem?
Because of your problem, do you have difficulty getting into or out of bed?
Does your problem significantly restrict your participation in social activities such as going
out to dinner, going to movies, dancing or parties?
Because of your problem, do you have difficulties in reading?
Does performing more ambitious activities like sports, dancing and household chores such as
sweeping or putting dishes away increase your problem?
Because of your problem, are you afraid to leave your home without having someone
accompany you?
Because of your problem, have you been embarrassed in front of others?
Because of your problem, do you avoid heights?
Because of your problem, is it difficult for you to do strenuous housework or yardwork?
Because of your problem, are you afraid people may think you are intoxicated?
Because of your problem, is it difficult for you to go for a walk by yourself?
Because of your problem, is it difficult to concentrate?
Because of your problem, is it difficult for you to walk around your house in the dark?
Because of your problem, are you afraid to stay at home alone?
Because of your problem, do you feel handicapped?
Has your problem placed stress on your relationships with members of your family or
friends?
Because of your problem, are you depressed?
Does your problem interfere with your job or household responsibilities?
38.2.2 Chronic Phase
The prognosis for a whiplash injury is usually favourable, and 90–95 % of patients
recover or have only minor remaining symptoms.
However, if symptoms persist more than 2 months after a whiplash injury, there
is a considerable risk of long-term problems.
Symptoms such as sleep impairment or memory and concentration problems as
well as signs of stress are reported approximately 25 % of the cases.
It is important to establish a correct diagnosis, both morphological (radiological)
and functional (motor and neurophysiological). QTF WAD grade has to be recon-
sidered. For example, symptoms seen in rhizopathy are usually dominated by sen-
sory symptoms in terms of pain and paraesthesia, while motor symptoms in terms
of clinically demonstrable paresis are often missing because single muscles are usu-
ally innervated by neighbouring nerve roots as well even if EMG changes can be
detected at the earliest within several weeks of the injury.
Recent studies focus on cervical ligament and facet joint lesions as specific fac-
tor of biomechanical chronicisation of WAD. It is uncommon that ligament injuries
can be detected in the acute phase after whiplash trauma, and it is uncommon or
radiologically verified instability to present later in the course.
MRI could be an important support to investigate patients developing WAD
chronicisation even if pronounced cervical flexor muscles are uncommon.
The most important element of late assessment is thus the identification of
patients who have developed serious consequences such as fractures, dislocations
(QTF WAD grade IV) or significant neurological damage (QTF WAD grade III) or
chronic pain or chronic functional disability.
Reduced cervical range of motion (ROM) is not necessarily associated with
ongoing disability after whiplash. Flattened cervical lordosis on X-rays is NOT
associated with ongoing pain.
Also crash aspects like direction of impact, speed of impact and seating position
in the car are not necessarily associated with ongoing pain and/or disability.
Older age, >75, and gender are not associated, too.
Chronicisation is due to the several physiological changes that occur in both the
peripheral and the central nervous system in acute and, when solved, long-term pain
associated with whiplash injury. Peripheral sensitisation is characterised by the
release of pain-producing substances, such as prostaglandins, bradykinins, cyto-
kines and substance P. Central sensitisation is characterised by the activation of the
NMDA receptor, decreased production of endogenous opioids, production of pain-
producing substances in the spinal cord and in the brain and activation of a neuronal
network that increases the pain impulse.
Although the same phenomena are observed in diffuse and chronic pain not asso-
ciated with whiplash [17], central sensitisation mechanisms have to be taken in
mind when planning the treatment of patient affected with WAD (see Chaps. 21 and
25) [18].
Chronic unsteadiness has to be extensively investigated. The background to the

dizziness is usually unclear but, even if there are diagnostic tests that can demon-
strate a connection between the dizziness and the whiplash trauma, extensive and
specific tests have to be performed with the aim of patient’s treatment. Posturography
allows a precise documentation of stance control disturbances (see Chap. 15);
Smooth Pursuit Neck Torsion Test (SPNTT) and Cranio-Corpo-Graphy (CCG) (see
Chap. 16) allow accurate documentation of cervico-cephalic dynamic control dis-
turbances either as oculomotor (SPNTT) and gait (CCG) disturbances.
Chronic dizziness requires also extensive investigation of eye movements (see
Chap. 18); chronic tinnitus, which could mask a not-investigated hearing loss,
requires an extensive audiological test battery (see Chap. 17).
Handicap induced by persistent dizziness may be quantified by means of the
Dizziness Handicap Inventory [15, 16].
Reassessment has to be planned at 2 weeks, 6 weeks and 3 months. If at 6 weeks
no significant improvement of pain or functional disability is noted despite multi-
modal therapeutic approach, the introduction of cognitive behavioural therapy
(CBT) is appropriate. In fact several studies indicate an increased occurrence of
post-traumatic stress disorder (PTSD) among people who have experienced a car
accident. According to the DSM-IV psychiatric diagnostic manual, PTSD is the
remaining condition that may follow acute stress disorder (ASD) that may occur
after an individual has been exposed to a traumatic event, if the symptoms occur
within 1–3 months. This remark highlights the importance of a correct management
of WAD in the acute and subacute phases. Thus, it is therefore important during
patient visit to gather information about previous conditions and examine the
patient’s current mental health. Psychiatric consultation is recommended in difficult
and/or complicated cases to minimise the risk of long-term PTSD.
Also minor psychological disorders like sleep impairment and anxiety have to be
adequately treated in WAD patients.
38.3 Treatment
38.3.1 Acute
Generally speaking, active exercise involving functional exercises and advice to

‘act/as/usual’ should be routinely undertaken. QTF WAD grade I and II patients
should also be advised that voluntary restriction of activity may delay recovery and
that it is important to focus on improvement in function.
In QTF WAD grade III, neurological and sensorial disorders have to be promptly
treated. Regarding the sensorial and/or functional symptoms that could lead to a
QTF WAD grade III classification, it is important to note that the QTF classification
states ‘symptoms and disorders that can be manifested in all grade include deafness,
dizziness, tinnitus, headache, memory loss, dysphagia, and temporomandibular
joint pain’.
Thus, for example, in the case of vertigo, positioning vertigo has to be diagnosed
and treated by means of the appropriate manoeuvres (see Chap. 23-I). In the case of
tinnitus and/or ear fullness, a hearing loss has to be immediately suspected and a
complete audiological battery performed: Pure Tone Audiometry is not sufficient to
exclude a hearing whiplash-associated damage (see Chap. 17).
38.3.1.1 Unsteadiness
Methylprednisolone, a drug with both neuroprotective and anti-inflammatory
effects, is reported to be associated with a significant reduction in disabling symp-
toms, total number of sick days and sick leave profile at 6 months after injury.
In QTF WAD grades I and II, exercise and mobilisation programmes to improve
kinaesthetic sensibility and coordination are indicated, together with educational
interventions in which patients are instructed about the nature and course of WAD
using personal communication: protect the neck from cold; walk daily; maintain
good posture; avoid lifting; and refrain from collar use after the first 2 days.
38.3.1.2 Pain
The successful management of acute pain reduces the risk of chronic pain.
In patients complaining moderately severe pain (VAS scale 5–6), irrespectively
of QTF WAD grade, paracetamol in combination with nonsteroidal anti-
inflammatory drug (NSAID) is indicated.
When pain intensity is severe (>7 in the VAS scale), a central-acting analgesic
combined with NSAID is necessary. They could be associated with an antihista-
mine for emesis even if the combination may improve central sedative effects.
Intra-articular injections and intravenous methylprednisolone have no support to be
used.
Severe pain in QTF WAD grade III has a very high risk of long-term symptoms.
Patients should completely refrain from work for at least 1 week until making a
return visit to the doctor for a strict and very careful follow-up.
Immobilisation with a soft collar is less effective than active mobilisation and no
more effective than advice to act as usual. In contrast, there is strong evidence that
active mobilisation is associated with reduced pain intensity and limited evidence
that mobilisation may also improve ROM. Collar use could be suggested for the first
2 days, no more than that. Cervical pillows have to be avoided.
Simple exercise programme promoting mobilisation of the neck is an effective
noninvasive intervention. Mobilisation programmes were differentiated from exer-
cise programmes in that exercise programmes had specific treatment aims (e.g.
strength and endurance), whereas mobilisation programmes were aimed at simply
increasing or maintaining mobility. Although long-term recovery may be unaffected
by either exercise or immobilisation in a soft collar during the acute phase of WAD,
it appears that exercise programmes are significantly more effective in reducing
pain intensity over both the short and medium term. Conversely, supplemental exer-
cise programmes added to mobilisation programmes may not be any more benefi-
cial than mobilisation programmes alone.
Multimodal therapy and active and passive repetitive movements (10 h over 6
weeks). Mobilisation (one 30 min session) has to be complemented with a home
exercise programme consisting of arm and shoulder movements eventually while
holding a 1.5 kg weight on the back in order to improve postural automatic align-
ment control (so-called torso weighting) and balance [19–21].
Patients who actually wore the collars as frequently as was stipulated had a
significantly higher risk of being disabled and/or having altered work ability
compared with patients in the mobilisation group. In terms of reducing pain at
2 months after injury, active therapy is significantly more effective than passive
therapy.
Educational interventions are interventions in which patients are instructed about
the nature and course of WAD using evidence-based pamphlets, videos or personal
communication. Advice to remain active (act as usual) is associated with signifi-
cantly better recovery in terms of a wide range of outcomes, including neck pain,
headache, memory and concentration.
PEMT decreases pain intensity and increases cervical ROM over the short term;
the evidence is insufficient to support the use of this treatment with confidence.
Laser acupuncture does not appear to be any more effective than placebo in the
treatment of acute WAD.
38.3.2 Subacute
Patients with whiplash do not constitute a homogeneous group; they do not have the
same type of injury and the same underlying causes of persistent or long-term prob-
lem that can be treated according to a single, across-the-board programme. The
hallmark should be the implementation of actions that promote rapid return to nor-
mal activity.
Interdisciplinary interventions may be more effective in reducing pain and sick
leave than passive physiotherapy modalities, although it is not clear enough which
components of such interventions are beneficial.
Patients who receive interdisciplinary treatment earlier are more likely to return
to work, but it is uncertain whether this simply reflects natural history or is a conse-
quence of the intervention.
Manipulation has short-term benefit to patients in the subacute stage of WAD
I–II. Thoracic and cervical spinal manipulations are effective in reducing pain and
improving cervical ROM (see Chap. 21).
The use of botulinum toxin injections during the subacute stage of WAD may
have a small treatment effect, and it does not appear that botulinum toxin injections
are any more effective than placebo.
The importance of physical therapy in patients with subacute whiplash injuries
varies significantly in relation to outcome parameter. Thus, a referral for physical
therapy may not be considered medically necessary for restoring range of motion,
yet it would appear to be extremely important from an economic standpoint in
reducing patients’ period of disability. From the patients’ point of view, however,
reduction in pain intensity is the most important goal. Here, prescription of ‘active’
physical therapy should be preferred. Considering all these factors, active physical
therapy is recommended for patients with QTF WAD grade II whiplash injuries as
the best option for achieving both therapeutic and economic objectives.
The effect of botulinum toxin A injections suggests that earlier treatment may
have some benefit in subacute WAD.
The serotonin-noradrenalin reuptake inhibitors (SNRIs) could be prescribed due
to their positive effects on pain and dizziness perception.
38.3.3 Chronic
Generally speaking, advice to act as usual, adequate reassurance and active exer-
cises involving functional exercises should be undertaken in QTF WAD grade I–II
patients. In QTF WAD grade III patients, neurological involvement has to be spe-
cifically treated.
38.3.3.1 Unsteadiness
Vestibular rehabilitation has to be instituted for persons experiencing dizziness in
the chronic phase. Planning the treatment requires subdividing patients into two
main groups:
1. Equilibrium disorders are mainly caused by a ‘quantitative’ decreasing of the
sensorial inputs or motor outputs or central integration of sensorimotor
patterns.
2. Equilibrium disorders are mainly caused by a ‘qualitative’ decreasing of central
sensorimotor integration in which the centre is not able to integrate sensorial
inputs comparing different sensorimotor patterns.
The treatment of disorders grouped in the first condition is mainly based on neu-
rorehabilitation. On the basis of responses to vestibular battery examination, excit-
atory (nicergoline, ginkgo biloba, piracetam) or inhibitory drugs (cinnarizine,
flunarizine) may be employed, too. On the basis of general vascular conditions,
some pathogenetic (aspirin, ticlopidine) drugs are associated.
In these patients neurorehabilitation (see Chap. 23) increases the activity of good
peripheral inputs acting on sensorial and motor redundance. Prognostic evaluation
is based on three specific goals: (1) the primary damage, the structural lesion of one
or more equilibrium subsystem; (2) the secondary damage, functional imbalance of
subsystems not directly involved by the lesion such as equilibrium disorders caused
by post-lesional postural syndromes; and (3) the tertiary damage, the crystalisation
of pathological sensorimotor patterns and/or psychological avoiding behaviours.
Rehabilitation is likely pointed toward limiting the primary damage, reducing
the secondary damage and avoiding the tertiary damage.
Rehabilitation is based either on peripheral sensorial and motor redundance or
on central spontaneous compensation mechanisms: functional sensorial substitu-
tion, structural reorganisation, recalibration of sensorimotor patterns and internu-
clear inhibition. Drugs are given to increase neural plasticity by means of axonal
sprouting and reorganisation of neural networks.
Weakness of ankle joint muscles, loss of ankle sensation and reduced mobility of
the ankles are contraindications for movement strategy training unless the underly-
ing physiological factors are also addressed.
Contraindications to teaching appropriate use of hip movements might include

weakness or loss of mobility about the hip joints. There is also clinical evidence
suggesting that patients with profound loss of peripheral vestibular function cannot
effectively coordinate hip movements and that training in these cases is ineffective.
The treatment of disorders grouped in the second condition is mainly based on
combination of rehabilitation and drugs with the aim of regaining correct balance
subsystem interconnection [22, 23].
The different behaviour of the two groups of equilibrium pathological systems is
caused by the pre-lesional characteristics of the patient, the quantitative characteris-
tics of the lesion, the qualitative characteristics of the disease and the side of
lesion(s).
Chronic WAD and dizziness in a vestibular rehabilitation programme twice a
week for 6 weeks and a 4-week home exercise programme consisting of slow eye-
head-neck coordination exercises twice daily. Different balance measures (tandem
standing and standing on one leg, both performed with eyes open and eyes closed)
and the Dizziness Handicap Inventory have to be assessed at baseline, 6 weeks and
3 months.
A 6-week programme aimed at stimulating the vestibular system is significantly
more effective than no treatment in increasing postural control and reducing self-
perceived handicap. Physiotherapy programme consists of soft tissue treatment,
isometric and isotonic exercises and advice regarding relaxation techniques, posture
and home exercise.
38.3.3.2 Pain
Collar immobilisation, cervical pillows and prescribed rest have to be avoided.
Intra-articular steroid injections and analgesic injections are not recommended.
Different treatments may be considered: exercise programmes, interdisciplinary
interventions, manipulations, pharmacological interventions and alternative treat-
ments (including myofeedback training and other alternative therapies).
Graded exercise with advice in a 4-week exercise programme has significantly
greater gains in pain intensity and pain bothersomeness, and functional ability exer-
cise programmes provided during the chronic phase of WAD are effective in relieving
pain, although it does not appear that these gains are maintained over the long term.
The programme consists of learning basic and applied skills and application and
generalisation of those skills in everyday activities with exercises to enhance mus-
cular stabilisation of the neck, shoulder mobility, body posture and arm muscle
strength.
In the case of temporomandibular disorders, therapeutic jaw exercises are sub-
stantially ineffective in reducing pain (see Chap. 11) if not combined with adequate
dentistry treatment such as stabilisation splint.
Changes in self-rated pain is significantly greater for patients treated by multi-
modal physiotherapy group in a 10-week intervention consisting of either a self-
management programme (education and information about exercise) or a multimodal
physiotherapy programme (including low-load exercises, low-velocity mobilising

techniques and education and assurance).
Groups that receive also home training report significantly less pain during rest
and less fatigue in the final week of treatment.
Trigger point treatment is effective in reducing pain. Injection-based interven-
tions may use both sterile water and saline. Sterile water injection or simple dry
needling results in significantly less mean pain distress and greater cervical mobility
immediately postinjection.
In selected subjects Botox may be used in order to obtain significant improve-
ments in terms of both pain intensity and cervical ROM.
Cognitive behavioural therapy (CBT) is aimed at promoting the acceptance of
pain and distress, when combined with physiotherapy. In severe disabling WAD,
CBT allows greater improvements in terms of pain disability, life satisfaction, kine-
siophobia, depressive symptomology and psychological flexibility.
Melatonin may be particularly useful in the treatment of chronic whiplash-
related sleep disturbance especially in older subjects [24]. Melatonin is involved in
synchronising circadian rhythms, and in healthy individuals, melatonin levels begin
to rise between 20:00 and 21:30. Treatment is not associated with reductions in pain
or any of the cognitive deficits associated with delayed melatonin onset but with
improvement of balance dizziness and tinnitus [25, 26].
In chronic QTF WAD grade III, fluoroscopically guided cervical selective nerve
root blocks using the corticosteroid solution or ‘joint regeneration’ (dextrose and
lidocaine intra-articular) therapy may reduce whiplash-related pain and disability,
in addition to physical therapy.
In shoulder chronic pain with both a positive impingement sign and a positive
analgesic block response of a painful shoulder, the programme is subacromial space
corticosteroid (40 mg methylprednisolone acetate) injections in conjunction with
physiotherapy programme designed to correct scapulothoracic rhythmic dysfunc-
tion and strengthen the rotator cuff muscle. This approach may be effective for
patients with late-onset shoulder pain.
For patients with chronic WAD who do not respond to conventional treat-
ments, it appears that radiofrequency neurotomy (RFN) may be the most effec-
tive treatment option, lesioning the cervical medial branches or third occipital
nerve for headache. Complications are lasting pain and/or numbness following
surgery; ataxia was a regular side effect of third occipital neurotomy. Pain refrac-
tory to the initial treatment (less than 30 days relief) did not respond to a second
treatment.
Epidural blood patch (EBP) is the therapy of choice in patients with chronic
WAD with a suspected cerebrospinal fluid (CSF) leak. Suspecting symptoms are
headache, memory, dizziness, visual impairment, cervical pain, nausea and auditory
symptoms. They may be significantly reduced 1 week following treatment.
However, the association of a CSF leak with chronic WAD has never been
established.
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Index
A Cervical spine, 2, 3, 24, 27, 29, 31, 39, 60,

Abducting ophtalmoplegia, 251–255 65–71, 82, 90–92, 98, 100, 103, 104,
Accelerometers, 37, 134, 135, 205–207, 119, 122, 128–134, 140,
285, 334, 339 174, 181, 194, 210, 217, 235,
Acupuncture, 275, 276, 278, 355–378, 394 237, 260, 261, 276, 291, 294–300, 322,
Alar ligaments, 68, 69 385, 386
Anatomy, 17–24, 119, 248, 377 Cervical tinnitus, 140
Ataxia, 7, 112, 162, 172, 179, 181, 194, 266, Cervico-ocular reflex (COR), 80, 161, 214,
343–348, 397 217–219
Attention, 1, 5, 40, 56, 57, 79, 82, 91–93, 104, Chinese medicine, 355–378
133, 139, 143, 145–149, 154–156, 162, Cognitive impairment, 93, 133
169, 230, 238, 266, 272, 281, 282, 292, Cognitive symptoms, 4, 57, 155
297, 308, 331, 347, 348 Compensation hypothesis, 61
Auricola, 356 Concerning, 27, 79, 83, 86, 118, 128, 144,
Autonomic system, 107, 108 168, 176, 181, 215, 236, 255, 261, 276,
282, 286, 292
Cranio-Corpo-Graphy (CCG), 198–206,
B 390, 392
B10, 358m 363m 371 CT scan, 48–50, 68, 72, 353, 385
Balance, 77–79, 92, 98, 120, 122, 132, 133,
153, 155, 156, 171–173, 176, 179–182,
189, 191, 193, 194, 207, 208, 214, 217, D
225, 233, 234, 237, 238, 265, 277, 278, Delos, 134, 135, 205, 272, 273, 334,
284, 292, 309, 310, 313, 327, 331, 332, 338–340
334–340, 343, 346–348, 374, 376–378, Disturbances of TMM, 360–367
394, 396, 397 Dizziness, 1, 6, 55, 56, 58, 59, 92, 108, 112,
Balance training, 277 120, 123, 127, 131, 153–158, 201, 209,
BioRid dummy, 32 210, 213, 219, 223–225, 234–237, 254,
Body sway, 163, 166–169, 171, 179, 260, 262, 296, 298, 306, 308–313, 318,
180, 185, 200 319, 321, 324, 328, 372, 378, 385,
Botox, 261, 397 390–393, 395–397
Brain natriuretic peptide (BNP), 356 Duplex sonography, 71–72
By heart exactly by the ventricles, 356 Dynamic posturography, 185–195, 278
C E
CARET, 275–278 Electrical stimulation, 80, 275, 315–319,
Centre of mass (COM), 100, 167, 333 321–324, 335
Centre of pressure (COP), 167, 172, 180 Electromyography (EMG), 101, 102, 113, 169,
Cervical pain, 260, 264, 286, 291, 397 225, 261, 347, 391

DOI 10.1007/978-88-470-5486-8, © Springer-Verlag Italia 2014
402 Index
Electrooculography (EOG), 209, 210, 234 Leads, 2, 3, 5, 6, 13, 22, 23, 30, 41, 51,
Electrovestibulography, (EVG), 224–231 57–60, 69, 78, 82, 83, 92, 96,
Equilibrium, 4–6, 79, 111, 123, 147, 153–163, 104, 108, 112, 113, 122, 123,
179, 180, 188, 189, 193, 194, 198, 200, 145, 153, 154, 193, 198, 201,
207, 223, 262–263, 273, 282, 284–288, 205, 214, 218, 219, 223, 234,
305–312, 319, 324, 330, 347, 373–377, 235, 259, 260, 266, 284, 305,
395, 396 306, 317, 378, 383, 398
Equitest, 6, 168, 169, 180, 187–189, 193, 194 Liberatory manoeuvres, 307
Evoked potentials, 91, 223–231, 390 Luo Vessel of Dumai, 371
F M
Facet joints, 39, 66, 67, 82, 83, 90, 91, 391 Magnetic resonance imaging (MRI), 45, 48,
Fasciculus longitudinalis medialis (FLM), 4 50, 57, 66, 68–70, 72, 91, 98, 203, 225,
Fine postural system, 95, 96, 99 291, 385, 391
Forming, 18, 19, 23, 78, 85 Manipulations, 23, 51, 132, 140, 145, 261,
Fourier analysis, 180, 181 274, 282–287, 301, 394, 396
Manual medicine, 123, 142, 143, 145,
281–288
G Meridians, 356–371
Greater occipital neuralgia, 56, 57 Motor vehicle collisions (MVC), 13, 14, 27,
41, 53, 55, 89, 117, 130, 259, 383
H
Headache, 44, 55–57, 98, 112, 117, 119, 131, N
133, 134, 143, 155, 235–237, 242, Neck
259–262, 266, 358, 365, 378, 393, 394, model, 2
397 pain, 1, 13, 15, 23, 30, 44, 45, 47, 55–57,
Head stabilization, 197, 200, 201, 206, 207, 309 66–70, 89, 90, 97, 98, 101, 118, 124,
Head-to-trunk stabilization, 200, 206 127, 172, 176, 179, 181, 201, 210, 211,
Hearing loss, 82, 83, 140, 141, 144, 155, 219, 242, 259–263, 292, 293, 365, 384,
213, 219, 225, 230, 248, 363, 384, 386, 394
385, 392, 393 sprain, 91, 103, 293
Helkimo index, 123 vibration, 316, 318, 324
Helmet headache, 363 Nystagmus, 92, 159–162, 214–217, 225, 233,
H-reflex, 321–324 235, 236, 241–249, 251, 252, 263, 264,
Hypocondralgia, 366 266, 282, 308, 318, 319
I O
Incidence, 13, 14, 23, 55, 56, 58, 59, 61, 96, Ocular disturbances, 59
97, 100, 118, 127, 129, 130, 133, 135, Optokinetic nystagmus (OKN), 161, 233,
155, 223, 238, 241 243–248, 252, 253, 319
Inner ear, 59, 78, 82–87, 90, 92, 108, 140, Oropharynx, 70, 71
141, 193, 213–220, 223, 225, Orthopaedic collar, 270–272
230, 263, 291 Oscillating platform, 327–332, 334
Interdisciplinary approach, 2 Otoneurology, 157, 163, 213, 347
Internal jugular veins (IJVs), 23, 24, 85–87
Internuclear ophthalmoplegia (INO), 251, 253,
255, 264, 395 P
Pain, 1, 13, 23, 30, 43, 55, 65, 82, 89, 97, 107,
117, 127, 139, 155, 172, 193, 200, 219,
L 235, 242, 259, 269, 281, 291, 317, 352,
L10, 367 355–372, 378, 384
Laser, 124, 274, 275, 372, 378, 394 Para-MLF, 253, 255
Index 403
Paresthesias, 1, 3, 44, 48, 55, 56, 59–60, 89, S

155, 159, 386 Saccades, 209, 233–238, 252, 253, 255
Paroxysmal positional vertigo (PPV), 58, 178, Scarpa’s, 360, 361
217, 223–231, 318, 385 Secondary meridians, 357
Pectoral energy, 357 Skitter, 327–330
Perceived stress questionnaire (PSQ), 144, Sleep disturbances, 44, 56, 58, 92, 397
145, 149 Smooth pursuit, 59, 157, 159, 208–211,
Perceptive surfaces, 351, 353 233–238, 252, 253, 319, 390, 392
Peripheral neural lesion, 93 Soft tissue lesion, 2, 43
Pharmacotherapy, 306, 310, 384 Somatic tinnitus, 139–149
Physical exercise, 140, 144, 145, 269, 270, Spinal cord, 21, 22, 56, 57, 60, 80, 91,
274, 310 108–110, 113, 114, 128, 129, 131, 132,
Polytrauma, 72, 343, 351–353 224, 272, 273, 321, 343, 344, 368, 378,
Poly-traumatic injuries, 72, 343, 351–352 385, 392
Post-concussional syndrome, 92 Sport injuries, 130
Postero-superior, 84 Stabilometry, 98, 124, 176, 177, 278
Posture, 6, 24, 51, 65, 72, 78, 79, 87, 92, Stepping test, 96, 162, 198, 200, 206
96, 98, 100, 121–122, 124, 134, 147, Stomatognathic, 117, 120, 124, 142, 143
158–159, 171, 172, 180,
185, 186, 192, 193, 197, 198, 200, 201,
269, 271, 273, 276, 309, 315, 330, 331, T
343, 345–347, 373, 374, 377, 393, 396 Temporomandibular disorders (TMDs),
Posture gait, 162–163, 176, 181, 182, 266, 117–125, 143, 396
309, 346–348, 390, 392 Temporomandibular joint (TMJ), 1, 82–85,
Posturography, 124, 134, 135, 142, 167–169, 117–124, 140–143, 159, 393
171–182, 185–195, 278, 374, 377, Tendino-muscular meridian (TMM), 357–371
390, 392 Tetra-ataxiometry, 179, 181
Prevalence, 6, 57, 58, 118, 175, 178, 194, 236, Third occipital headache, 56, 57
319, 344, 345, 373–375 Thoracic outlet syndrome (TOS), 44, 60
Psychiatric disorders, 55, 56, 58 Tinnitus, 1, 5, 44, 65, 82, 83, 139–149, 155, 213,
217–220, 242, 248, 385, 392, 393, 397
Tinnitus Cognitive Questionnaire (TCQ),
Q 143, 145, 149
Quebec task force (QTF), 13, 15, 55, 89, 128, Tinnitus Reaction Questionnaire (TRQ),
236, 259, 286, 288, 292–294, 301, 368, 143–145, 149
383, 384 TMJ derangement, 56, 57
Quebec task force rehabilitation, 395 Trigeminus nerve, 157
Trunk sway, 181–182, 207
R
Radiculopathy, 56, 60, 131 V
Radiography, 91, 103, 386 Venous blood flow, 23, 24, 87
Rear impact, 30, 32, 33, 37, 39–41, 51, 60, 91 Venous drainage, 24, 78, 85–87
Regular meridian, 357, 360, 365, 371 Vertebral artery, 5, 17–20, 23, 56, 72, 81,
Regular meridian of GB, 360, 371 84–86, 92, 140, 210, 217, 223,
Rehabilitation, 7, 53, 102, 124, 133, 173, 267, 274, 286
270–272, 275, 278, 291–301, 305–313, Vertebral veins (VVs), 23, 24, 86
317, 319, 334, 340, 344, 345, 347, 348, Vertigo, 1, 5, 6, 51, 58, 65, 66, 79, 82, 83, 108,
351–353, 395, 396 111, 112, 139, 153–156, 158, 172, 173,
Represent, 14, 17, 18, 22–24, 40, 43, 47, 176, 193, 198, 213–215, 223–231,
57, 58, 78, 86, 87, 117, 124, 129, 234–236, 242, 254, 260, 262–267, 274,
143–145, 149, 166, 167, 199, 200, 277, 292, 296, 298, 305–308, 310, 318,
203, 207, 233, 293, 295, 318, 334, 319, 321, 324, 373, 377, 378, 384, 385,
336, 338, 345, 351, 383 390, 393
Risk factors, 14, 15, 60, 117, 129, 136, 386 Vertigo dizziness, 154, 155, 158, 260, 296, 298
404 Index
Vestibular electrical stimulation, 315–319, W

321–324, 333 Weakness, 13, 55, 56, 60–61, 260, 293, 297,
Vestibular evoked myogenic potentials 335, 384, 385, 395, 396, 1289
(VEMPs), 224–231 Whiplash,
Vestibular rehabilitation, 305–313, 395, 396 benign paroxysmal positional vertigo
Vestibular system, 4, 5, 77, 79, 154, 169, (BPPV), 58, 224, 307
171, 172, 189, 198, 205, 214, posture/posturology/posturography,
215, 241, 262–266, 272, 308, 6, 24, 31, 51, 59, 65, 77, 92, 95–104,
316, 335, 343, 396 108, 121, 131, 142,
Vestibulo-collic reflex (VCR), 79, 80, 224 156, 165–169, 171–182, 185–195, 197,
Vestibulo-ocular reflex (VOR), 79, 80, 159, 214, 238, 265, 269, 284,
214–219, 233, 236, 237, 243–249, 252, 306, 315, 321, 330, 333–340,
253, 318, 319, 373 343, 352, 373, 385
Vestibulo-spinal reflexes (VSR), 79, 80, 172, Whiplash associated disorders (WAD), 2,
176, 179, 318, 319, 373, 377 13–15, 45, 55, 68, 89, 97, 107, 118,
Video-oculography, 234 128, 141, 172, 198, 214, 224, 234,
Visual feedback, 272, 273, 319, 328, 330, 259–267, 269, 281–286, 292, 340, 370,
333–340 383–397
Visual symptoms, 55, 56, 59, 235 Wii, 340
Visuo-vestibular interaction, 241–249
Visuo vestibularocularreflex (VVOR),
243–248, 252, 253, 255, 319 X
Voluntary eye movements, 233–238 X-rays, 45, 66–67, 72, 391

Whiplash Injuries

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Whiplash Injuries

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Whiplash

Dario C. Alpini · Guido Brugnoni

ISBN 978-88-470-5485-1 ISBN 978-88-470-5486-8 (eBook)

Library of Congress Control Number: 2014932997

© Springer-Verlag Italia 2014

Printed on acid-free paper

Springer is part of Springer Science+Business Media (www.springer.com)

I have dedicated my early researches to the study of learning disturbances and

Prof. Reuven Kohen-Ratz,

1 Whiplash: An Interdisciplinary Challenge . . . . . . . . . . . . . . . . . . . . . 1

Part I General Aspects

2 Epidemiology of Whiplash-Associated Disorders . . . . . . . . . . . . . . . . 13

8 The Vestibulo-vertebral Functional Unit . . . . . . . . . . . . . . . . . . . . . . . 77

10 The Contribution of Posturology in Whiplash Injuries . . . . . . . . . . . 95

Part III Evaluation

15 Anamnesis and Clinical Evaluation of Whiplash-Associated

23 Whiplash Effects on Brain: Optokinetic Nystagmus

25 Pharmacological Treatment of Whiplash-Associated

35 Rehabilitation in Polytrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351

Part V Conclusive Remarks

38 Management and Treatment of WAD Patients:

Definitions of whiplash syndrome are controversial. Generally speaking, the

D.C. Alpini et al. (eds.), Whiplash Injuries, 1

Table 1.1 Abbreviated AIS-Code Injury

The different combinations of symptoms lead to different syndromes so described

dysregulation causing a specific activation of nociceptive inputs and consequent

This circuitry is the anatomo-neurophysiological basis needed to understand

neuroasthenic symptoms including tinnitus, dysphasia, nausea, unsteadiness, and

Rehabilitation is generally the treatment of choice either in acute or in chronic

Until recently, there was no consensus on the definition of whiplash. According to

D.C. Alpini et al. (eds.), Whiplash Injuries, 13

2.1 Factors Associated with WAD

Younger persons (aged 18–23) seem to be at greater risk of making insurance

6. Richter M, Otte E, Pohlemann T et al (2000) Whiplash-type neck distortion in restrained car

D.C. Alpini et al. (eds.), Whiplash Injuries, 17

Fig. 3.4 Conjugate foramen

P.L. Ardoino and F. Ioppolo

4.2 Accident Typology at the Origin of the Whiplash

D.C. Alpini et al. (eds.), Whiplash Injuries, 27

Fig. 4.2 Injury mechanism

4.3 Whiplash Injury Mechanism

4.4 Technical and Structural Limits

4.5 Phases of the Collision

A stereotypical kinematic and neuromuscular response has been observed in human

4.5.1 First Phase

Higher or lower stiffness of the vehicles brings a different degree of deformation

4.5.2 Second Phase

Fig. 4.3 Rear-impact

Fig. 4.4 Time histories of the passenger compartment

4.5.3 Third Phase

Fig. 4.5 Hybrid III instrumentation

Fig. 4.6 Pelvis, chest, head time histories

Fig. 4.7 Pelvis, chest velocity vs time

Fig. 4.8 Chest, head velocity vs time

Neck – axial load

Fig. 4.9 Head and neck loadings

Fig. 4.10 Neck loadings and kinematics

4.6 Angled Rear-End Collisions

Fig. 4.11 Centered-angled-rear collision; CG center of gravity

4.7 Out-of-Position Whiplash

Rear-impact collisions at low speed are a leading cause of economic costs

5.2 Clinical Course

In an acute phase right after the trauma, the symptomatology is characterized by